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Carlo D. Franco, MD
Chairman Orthopedic Anesthesia
JHS Hospital of Cook County
www.CookCountyRegional.com
Chicago, IL
Third Edition
2008
This manual is intended for Anesthesiology Residents, Nurse Anesthetists and
Faculty of the Department of Anesthesiology and Pain Management, Cook County
Hospital of Chicago. The writing in these pages reflects the author’s own experience, as
well as his understanding and interpretation of the available literature. The author made
every effort to give proper credit to outside sources.
The persons depicted in pictures in this manual gave their written permission to
the author, to have their photographs taken for the purpose of teaching. Their decision
was voluntary and did not involve compensation of any kind. The photographs of cadaver
material shown in these pages, come from dissections performed by the author in the
Anatomy Laboratory of Rush University Medical Center in Chicago, in compliance with
Rush University guidelines, as well as State and Federal laws and regulations.
Care has been taken to confirm the accuracy of the information presented.
However, the author is not responsible for errors or omissions, or for any consequences
resulting from application of the information and techniques in this manual, and makes
no warranty, expressed or implied, with respect to the contents of it.
This manual is in accordance with current recommendations, as of April 2008.
However, recommendations and guidelines change, therefore the reader is urged to check
for new indications, warnings and precautions.
2|Page
To my residents,
who make my coming to work
intellectually challenging and pleasurable
and
to the memory of my father
3|Page
CONTENTS
Chapter 1: Introduction
General considerations………………………………………………………………….. 8
Patient selection and premedication……………………………………………………. 8
Monitoring……………………………………………………………………………..… 9
Outcome issues…………………………………………………........................................9
Airway and regional anesthesia………………………………………………………….11
References……………………………………………………………………………..…12
Historical perspective………………..…………………………………………………...14
Chemical structure ……………………………………………………………………....15
Structure-activity relationship………………………….………………………………...16
Mechanism of action and Na+ channels……………….………………………………....17
Frequency-dependent blockade…..………………….…………………………………..17
Pregnancy and local anesthetics……………………………………………………….....18
Fiber size and pattern of blockade………………….…………………………………....18
Modulating local anesthetic action…….………………………………………………...19
Local anesthetics additives…………….……………………….………………………..20
Metabolism………………………….………………………….
……………………......23Dibucaine
number…………………………………………………………………...…...24
Toxicity…………………………………………………….……………………….........25
Tumescent anesthesia……………………………………………………………….........26
Toxic plasma concentrations………………………………………………………..…....26
Toxicity management……………………………………………………………….........27
Lipid emulsion……………………………………………………………………....…...27
Maximum dose…………………………………………………………………………...28
Methemoglobinemia……………………………………………………………….....….29
Allergy ………………………………………………………………………………......29
Profile summary of selected agents………………………………………..……….…....30
References……………………………………………………………………………......34
Spinal anesthesia
Anatomy………………………………………………………….........................37
Cerebrospinal fluid………………………………………………………….........38
Site of action and indications…………………………………….........................39
Baricity………………………………………………………………………..….39
Determinants of spread………………………………………………………..…39
Techniques (median, paramedian, Taylor’s)………………………………..…...40
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Anesthesia duration…………………………………………………………........31
Side effects and complications……………………………………………..…….41
Other physiological effects……………………………………………………....42
Postdural puncture headache………………………………………………….….43
Transient neurological symptoms……………………………………………......44
Cauda equina syndrome…………………………………………………….........45
Back pain ………………………………………………………………….…….45
Spinal in the outpatient………………………………………………………..…46
Intrathecal adjuncts………………………………………………........................46
Epidural Anesthesia
Anatomy………………………………………………………….........................47
Blockade characteristics………………………………………….........................47
Spread of local anesthetics……………………………………….........................47
Techniques……………………………………………………………………….47
Type of needles and catheters……………………………………………………48
Test dose…………………………………………………………........................48
Activating an epidural………………………………………………………........48
References…………………………………………………………………………......…49
Introduction…………………………………………………………………………........51
Guidelines summary…………………………………………………………………......52
2002 consensus highlights………………………………………………………...……..52
New anticoagulants…………………………………………………………………........57
References………………………………………………………………………………..58
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Axillary block………………………………………………………………………...….87
References………………………………………………………………………………..90
Anatomy……………………………………………………………………………….…92
Subgluteal fold…………………………………………………………………………...94
Male and female pelvis issue…………………………………………………………….95
Lateral femoral cutaneous nerve block…………………………………………………..96
Femoral block…………………………………………………………………………....97
Obturator nerve block………………………………………………………………....…99
Lumbar plexus block…………………………………………………………………....100
Sciatic nerve block, classic (Labat-Winnie)…………………………………………....102
Sciatic nerve block, Franco’s…………………………………………………………...104
Sciatic subgluteal nerve block, di Benedetto’s………………………………………....107
Sciatic subgluteal nerve block, Franco’s…………………………………………….....109
Popliteal nerve block, Franco’s………………………………………………………....111
Popliteal nerve block, lateral approach………………………………………………....113
References………………………………………………………………………….…...114
Introduction……………………………………………………………………………..116
Benefits…………………………………………………………………………………116
Stimulating versus non-stimulating catheters………………………………………….117
Catheter-related problems………………………………………………………………117
References……………………………………………………………………………....118
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CHAPTER 1
INTRODUCTION
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General considerations
The type of anesthesia for any procedure must be tailored to every individual
patient. There are patients who in general are not good candidates for regional anesthesia,
especially if they remain awake (e.g., drug abusers, pediatric patients). On the other hand
we have a vast and successful experience with peripheral nerve blocks on drug abusers
and some pediatric patients, confirming that each case must be individually evaluated.
Judicious use of sedation increases patient’s cooperation and acceptance. Sedation
should be used to calm anxiety, but not to turn the patient unconscious or otherwise
unresponsive. This is especially true in blocks performed close to the neuraxis, like
interscalene blocks and lumbar plexus blocks. Keeping the patient lightly sedated, but
awake and cooperative, makes the procedure easier for both the patient and the
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anesthesiologist. A conscious and cooperative patient may also potentially decrease the
chances of complications (e.g., pain at injection, early subjective symptoms indicating
impending systemic toxicity, etc).
Monitoring
Every nerve block, whether it is performed in holding area, OR, PACU or office,
must be treated as potentially dangerous. Monitoring blood pressure, heart rate and pulse
oxymetry, as well as the establishment of IV access must always be considered.
Supplemental oxygen should be given especially when sedation is being used.
Resuscitation equipment, including oxygen, ambu bag, airways of different sizes,
intubation equipment and tubes, along with appropriate resuscitation drugs and suction
capabilities, must always be readily available.
A clear strategy to deal with and treat complications must be in place. It is always
advisable, before starting a technique, to leave room at the head of the bed for the
anesthesiologist to manage the patient’s airway, should that become necessary.
Familiarity with the surroundings helps when dealing with emergencies.
Outcome
Is regional anesthesia safer than general anesthesia?
Every discussion on regional anesthesia must address the issue of its relative
safety compared to general anesthesia. Despite several studies suggesting it and an
intuitive feeling that regional anesthesia seems “safer’ than general anesthesia, no definite
and general answer can be given. The inability to give a clear answer comes from
insufficient data. Most of the outcome studies available to us, have compared the relative
benefits of neuraxial anesthesia (spinal or epidural) versus general anesthesia in intra
abdominal surgery. Most of the studies lack the power (number of cases) to be able to see
a true difference, if it existed, and most of them are retrospective. Lack of randomization
raises the possibility of bias at the time of technique selection (i.e., sicker patients
receiving more regional anesthesia).
Other problems have to do with the parameter chosen for comparison. To
compare mortality for example, the sample would have to be extremely large in order to
find a statistically significant difference, since mortality under any type of anesthesia is
extremely low. Other parameters like DVT, myocardial infarction, pneumonia seem more
adequate for comparison, but their rates vary according to the procedure and not just type
of anesthesia.
The physiological response to the stress of surgery or “surgical stress response”
involves release of local and central mediators leading to increased levels of, among
others, cathecolamines, cortisol, aldosterone and renin. It is also frequently associated
with hypercoagulability, immune response depression and protein wasting. The release of
local tissue inflammatory factors like cytokines and interleukins can be partially blocked
by non-steroidal anti-inflammatory drugs and peripheral nerve blocks using local
anesthetics. The central response, responsible for the release of cathecolamines and
cortisol, can only be blocked by neuraxial blocks using local anesthetics. Determination
of hormonal markers of stress can be demonstrated after general anesthesia and after
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certain regional anesthesia techniques. However, its impact on morbidity has not been
clearly established. If physiological parameters are measured (e.g., PO2, O2 sat) there is
also some evidence that the values obtained are frequently better after regional than
general anesthesia. However, the real impact that better postoperative physiological
parameters have on morbidity is not clear.
Nonetheless, there seems to be some agreement that regional anesthesia improves
the outcome of selective surgical procedures in a number of different ways, including
decreased rates of DVT, PE and blood loss.
Surgeries most associated with improved outcome after regional anesthesia include:
1. Hip surgery (hip fracture surgery and total hip arthroplasty): rates of DVT, PE and
blood loss are reduced after neuraxial anesthesia. The mechanism is unknown, but
may involve better peripheral circulation and less stasis.
Mortality rates also have been shown to be significantly lower with epidural
anesthesia as compared to general anesthesia.
2. Total knee arthroplasty: rates of DVT and PE are lower with neuraxial anesthesia.
3. Prostatectomy: similar reduction rates in DVT and PE and may also involve better
peripheral circulation and decreased venous stasis.
4. Peripheral vascular surgery: epidural anesthesia and postoperative epidural
analgesia have shown to improve graft patency after peripheral vascular surgery,
but does not seem to improve outcome after intra-abdominal vascular surgery.
Mechanism is not clear. Improve runoff due to vasodilatation or preservation of
normal coagulation has been mentioned.
5. Colon surgery: postoperative thoracic epidural analgesia with local anesthetics
has shown to enhance colonic activity after colon resection. If narcotics are used
in conjunction with local anesthetics this beneficial effect is lost.
1. Upper abdominal and thoracic surgery, this is despite the fact that better pain
scores and times to extubation after regional anesthesia can be demonstrated.
2. Upper and lower extremity surgery: even though the patients receiving regional
anesthesia may have a higher degree of satisfaction and fewer side effects (nausea
and vomiting), especially immediately after surgery. This difference rapidly
disappears at 24 h.
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1. Overall mortality was about one third less in the neuraxial group (103 deaths/4871
patients versus 144/4688 patients, P=0.006). This decrease was observed
regardless of whether neuraxial was used alone or in combination with general
anesthesia.
2. DVT decreased by 44%
3. PE decreased by 55%
4. Transfusion requirement decreased by 50%
5. Pneumonia decreased by 39%
6. There were also reductions in myocardial infarction and renal failure.
The authors concluded that neuraxial blocks “reduce postoperative mortality and
other serious complications”, adding that it was not clear whether these effects were due
“solely to benefits of neuraxial blockade or partly to avoidance of general anaesthesia”.
Meta-analysis has the advantage of pooling large numbers, therefore infrequent
clinical events can be studied. However, it also means putting together trials from
different settings. They not only include data from different institutions, but also in some
cases different countries and cultures. It remains to be seen whether these very
encouraging results can be duplicated, and whether they could apply more generally to
regional anesthesia beyond neuraxial blocks (i.e., peripheral nerve blocks).
Other authors, like Christopher Wu from Johns Hopkins, have shown the benefits
of regional over general anesthesia, when non-traditional outcomes are measured. These
outcome parameters include patient satisfaction (including analgesia, prevention of
nausea and vomiting and discharge readiness), ability to undergo physical rehabilitation,
and cost. These so-called “soft” parameters are having increased importance in today’s
cost-conscious practice.
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References
1. Liu SS, Carpenter RL, Neal JM. Epidural anesthesia and analgesia. Their role in
postoperative outcome. Anesthesiology 1995; 82:1474-1506
2. Sharrock NE: Risk-Benefit Comparisons for Regional and General Anesthesia, In:
Finucane BT (ed), Complications of Regional Anesthesia. New York, Churchill
Livingstone, 1999, pp 31-38
3. Neal JM, McDonald SB. Regional Anesthesia and Analgesia: Outcome and Cost
Effectiveness. In: Neal JM, Mulroy MF, Liu SS (eds), Problems in Anesthesia,
Philadelphia, Lippincott, Williams & Wilkins, 2000, pp 188-198
4. Neal JM: Regional anesthesia and Outcome. In: Rathmell JP, Neal JM, Viscomi
CM (eds), Regional Anesthesia, The Requisites in Anesthesiology, Philadelphia,
Elsevier Mosby, 2004, pp 164-170
5. Rodgers A, Walker N, Schung S et al. Reduction of postoperative mortality and
morbidity with epidural or spinal anaesthesia: results from overview of
randomized trials. Br Med J, 2000; 321: 1493-504
6. Wu CL, Fleisher LA. Outcomes research in regional anesthesia and analgesia,
Anesth Analg 2000; 91: 1232-1242
7. Urban MK: Is Regional Anesthesia Superior to General Anesthesia for Hip
Surgery?, In: Fleisher LA (ed), Evidence-Based Practice of Anesthesiology.
Philadelphia, Saunders, 2004, pp267-269
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CHAPTER 2
LOCAL ANESTHETICS
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LOCAL ANESTHETICS
The cell membrane’s resting potential is negative and close to the potential
determined by potassium alone (-70 mV). During the transmission of an action potential,
Na+ moves into the cell through open Na+ channels depolarizing the membrane and
bringing its potential to -20 mV or more.
Local anesthetics are compounds that have the ability to interrupt the transmission
of the action potential in excitable membranes. They bind to specific receptors in the Na+
channels and their action, at clinically recommended doses, is reversible. Conduction can
still continue, although at a slower pace, with up to 90% of receptors blocked.
All local anesthetics are neurotoxic, if injected intraneurally, and the damage
caused is directly related to the degree of hydrostatic pressure reached inside the
axoplasma. Local anesthetics injected around nerves could also be toxic as result of the
concentration of the agent and the duration of the exposure (e.g., cauda equina after
intrathecal local anesthetics).
The local anesthetics available in clinical practice are usually racemic mixtures,
that is a mixture of both R and S enantiomers. Exceptions are lidocaine, levo-bupivacaine
and ropivacaine. The S isomer appears to have similar efficacy than the R isomer, but
lesser cardiac toxicity.
Historical perspective
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1885 Wood, in the United Kingdom, is credited with the introduction of conduction
anesthesia through hypodermic injection.
1897 Epinephrine is isolated by John Abel at Johns Hopkins Medical School.
1897 Braun in Germany relates cocaine toxicity with systemic absorption and advocates
the use of epinephrine.
1898 Bier is set to receive the first planned spinal anesthesia from his assistant
Hildebrandt. After CSF is obtained, the syringe is found not fit the needle and therefore
no injection could be performed. Bier then performs the first spinal anesthesia on
Hildebrandt using cocaine. They both experience the first spinal headaches.
1908 Bier introduces the intravenous peripheral nerve block (Bier block) with procaine.
1911 Hirschel performs the first percutaneous axillary block.
1911 Kulenkampff performs the first percutaneous supraclavicular block.
1922 Gaston Labat from France, a disciple of Pauchet, introduces in the US his book
“Regional Anesthesia Its Technic and Clinical Application”, the first manual of regional
anesthesia published in America.
1923 Labat founds the first American Society of Regional Anesthesia.
1953 Daniel Moore, from Virginia Mason Clinic in Seattle, publishes his book “Regional
Block”.
1975 Alon Winnie, L. Donald Bridenbaugh, Harold Carron, Jordan Katz, and P. Prithvi
Raj establish the current American Society of Regional Anesthesia (ASRA) in Chicago.
1976 The first ASRA meeting is held in Phoenix, Arizona.
1976 Regional Anesthesia Journal, volume 1, number 1 is published.
1983 Winnie introduces his book, Plexus Anesthesia, Perivascular Techniques of
Brachial Plexus Block.
1905 procaine; 1932 tetracaine; 1947 lidocaine; 1955 chloroprocaine (last ester
type that is still in clinical use); 1957 mepivacaine; 1963 bupivacaine; 1997 ropivacaine;
1999 levobupivacaine.
Local anesthetics are weak bases with a pka above 7.4 and poorly soluble in
water. They are commercially available as acidic solutions (pH 4-7) of hydrochloride
salts, which are hydrosoluble. A typical local anesthetic molecule is composed of two
parts, a benzene ring (lipid soluble, hydrophobic) and an ionizable amine group (water
soluble, hydrophilic). These two parts are linked by a chemical chain, which can be either
an ester (-CO-) or an amide (-HNC-). This is the basis for the classification of local
anesthetics as either esters or amides.
Injecting local anesthetics in the proximity of a nerve(s) triggers a sequential set
of events, which eventually culminates with the interaction of some of their molecules
with receptors located in the Na+ channels of nerve membranes. The injected local
anesthetic volume spreads initially by mass movement, moving across “points of least
resistance”, which do not necessarily lead into the desired nerve(s). This fact emphasizes
the importance of injecting in close proximity to the target nerve(s). The local anesthetic
15 | P a g e
solution then diffuses through tissues; each layer acting as a physical barrier. In the
process part of the solution gets absorbed into the circulation. Finally a small percentage
of the anesthetic reaches the target nerve membrane, at which point the different
physicochemical properties of the individual anesthetic will dictate the speed, duration
and nature of the interaction with the receptors.
1. Lipid solubility: determines both the potency and the duration of action of local
anesthetics, by facilitating their transfer through membranes and by keeping the
drug close to the site of action and away from metabolism. In addition, the local
anesthetic receptor site in Na+ channels is thought to be hydrophobic, so its
affinity for hydrophobic drugs is greater. Hydrophobicity also increases toxicity,
so the therapeutic index of more lipid soluble drugs is decreased.
2. Protein binding: local anesthetics are bound in large part to plasma and tissue
proteins. The bound portion is not pharmacologically active. The plasmatic
unbound fraction is responsible for systemic toxicity. The most important binding
proteins in plasma are albumins and alpha-1-acid glycoprotein (AAG). Although
albumin has a greater binding capacity than AAG, the latter has a greater affinity
for drugs with pka higher than 8, the case for most local anesthetics. Newborn
infants have very low concentration of AAG, only reaching adult values by 10
months of age. The elderly and debilitated also frequently have decreased levels
of albumin and other plasma proteins. These patient populations could be at
increased risk for toxicity.
On the other hand, AAG levels increase during stress and for several days
after the postoperative period. Higher levels of AAG lead to decreased levels of
unbound fraction of local anesthetics and a decreased potential for local anesthetic
toxicity. However, changes in protein binding are only clinically important for
drugs highly protein-bound, such as bupivacaine, which is 96% bound, and
sufentanil and alfentanil, which are both 92% bound (Booker et al, Br J Anaesth
1996; 76:365-8).
The fraction of drug bound to protein in plasma correlates with the
duration of action of local anesthetics: bupivacaine (95%) = ropivacaine (94%)>
tetracaine (85%) > mepivacaine (75%) > lidocaine 65%) > procaine (5%) and
2-chloroprocaine (negligible). This suggests that the binding site for the local
anesthetic molecule in the sodium channel receptor protein, may share a similar
sequence of amino acids with the plasma protein binding site.
Drugs as lidocaine, tetracaine, bupivacaine and morphine (e.g., DepoDur)
have been incorporated into liposomes to prolong their duration of action.
Liposomes are vesicles with two layers of phospholipids, which slow down the
release of the drug.
3. Pka: determines the ratio between the ionized (cationic) and the uncharged (base)
forms of the drug. The pka of local anesthetics ranges from 7.6 to 9.2. By
definition the pka is the pH at which 50% of the drug is ionized and 50% is
16 | P a g e
present as a base. The pka generally correlates with the speed of onset of most
local anesthetics. The closer the pka is to physiologic pH, the faster the onset. For
example, lidocaine with a pka of 7.7 is 25% non-ionized at pH 7.4. Its onset is
therefore faster than bupivacaine, whose pka of 8.1 makes it only 15% non-
ionized at that pH. One important exception is 2-chloroprocaine that, despite its
pka of 9.1, has a very rapid onset. This is usually attributed to the relatively high
concentrations used in clinical practice (3%) that are possible thanks to its low
toxicity. It is also claimed that 2-chloroprocaine has better “tissue penetrability”.
The non-charged hydrophobic fraction (B), which exists in equilibrium with the
hydrophilic charged portion (BH+), crosses the lipidic nerve membrane and initiates the
events that lead to Na+ channel blockade. Once inside the cell, the pka of the drug and the
intracellular pH dictate a new equilibrium between the two fractions. Because of the
relative more acidic intracellular environment, the relative proportion of charged fraction
(BH+) increases. This hydrophilic, charged fraction is the active form on the Na+ channel.
The Na+ channel is a protein structure that communicates the extracellular of the
nerve with its axoplasm. It consists of four repeating alpha subunits and two beta
subunits, beta-1 and beta-2. The alpha subunits are involved in ion movement and local
anesthetic activity. It is generally accepted that the main action of local anesthetics
involves interaction with specific binding sites within the Na+ channel. Local anesthetics
may also block to some degree calcium and potassium channels as well as N-methyl-
D-aspartate (NMDA) receptors. Local anesthetics do not ordinarily affect the membrane
resting potential.
The Na+ channels seem to exist in three different states, closed (resting), open and
inactivated. Under adequate stimulation, the protein molecules of the channel undergo
conformational changes, from the resting state to the ion-permeable state or open state,
allowing the inflow of extracellular Na+, which depolarizes the membrane. After a few
milliseconds the channel goes then through a transitional inactivated state, where the
proteins leave the channel closed and ion-impermeable. With repolarization the proteins
revert to their resting configuration.
Other drugs, like tricyclic antidepressants (amitriptyline), meperidine, volatile
anesthetics and ketamine, also exhibit Na+ channel-blocking properties. Tetrodotoxin and
other biotoxins also interact with the Na+ channels, although their actions are exerted on
the extracellular side of the channel.
Frequency-dependent blockade
Local anesthetics show more affinity for open Na+ channels. When a nerve is
experiencing a high frequency of depolarization, like during spontaneous pain or
voluntary muscle contractions, it becomes more sensitive to blockade, because the
chances of interaction, between local anesthetics molecules and Na+ channels, increase.
The concept of frequency-dependent blockade also explains the greater
susceptibility to blockade exhibited by small sensory fibers, as they generate long action
17 | P a g e
potential (5 ms) at high frequency. Motor fibers on the other hand generate short action
potentials (0.5 ms) at lower frequency making them more difficult to block.
As a general rule small nerve fibers are more susceptible to local anesthetics than
large fibers. However, other factors like myelinization and relative position of the fibers
within a nerve (mantle versus core) may also play a role. The depolarization in
myelinated fibers is saltatory. About three nodes of Ranvier need to be blocked in order
to block the transmission of the action potential.
The smallest nerve fibers are nonmyelinated and are blocked more readily than
larger myelinated fibers. However at similar size, myelinated fibers are blocked before
nonmyelinated fibers. In general autonomic fibers, small nonmyelinated C fibers
(mediating pain, temperature and touch), and small myelinated A delta fibers (mediating
pain and cold temperature) are blocked before A alpha, A beta and A gamma fibers
(motor, propioception, touch, and pressure).
It has been speculated that in large nerve trunks, motor fibers would be usually
located in the outer portion (mantle) of the nerve bundle, therefore more “accessible” to
local anesthetics. This would help explain why motor fibers tend to be blocked before
sensory fibers in large mixed nerves. In contrast, the frequency-dependence of local
anesthetic action would favor block of small sensory fibers, as they generate long action
potentials at high frequency, whereas motor fibers generate short action potentials at
lower frequency.
18 | P a g e
(Figure from Morgan’s Clinical Anesthesiology, 3rd edition, 2006, reproduced with permission)
The ionized fraction of local anesthetics is the active form in the Na+ channel,
although the rate-limiting step in this cascade is membrane penetration of local
anesthetics in its non-ionized form. Unfortunately, only a small proportion of local
anesthetic in solution exists in the non-ionized state. Changes in pH can theoretically
reduce the onset time by increasing its proportion. At a pH of 5.0 to 5.5 the cation/base
ratio is 1000:1, at a pH of 7.4 the same ratio becomes 60:40. The limiting factor for pH
adjustment is the solubility of the base form before reaching precipitation. The most lipid
soluble agents, like bupivacaine and ropivacaine, cannot be alkalinized above a pH of 6.5
because they precipitate.
DiFazio et al (Anesth Analg 1986:65; 760-64) demonstrated a more than 50%
decrease in onset of epidural anesthesia, when the pH of commercially available
lidocaine with epinephrine was raised from 4.5 to 7.2, by the addition of bicarbonate.
Capogna et al (Reg Anesth 1995; 20: 369-377) randomized 180 patients to study the
effects of alkalinizing lidocaine, mepivacaine and bupivacaine for nerve blocks. They
concluded that alkalinization of lidocaine and bupivacaine shortens the onset of epidural;
alkalinization of lidocaine shortens the onset of axillary block and alkalinization of
mepivacaine shortens the onset of sciatic/femoral blocks. However, when only small
changes in pH can be achieved, because of the limited solubility of the base, only small
decreases in onset time will occur, as when plain bupivacaine is alkalinized.
It is generally accepted that adding bicarbonate to local anesthetics, may speed the
onset of local anesthetics solutions that have epinephrine added by the manufacturer
19 | P a g e
(vials have a lower pH), while the effect would be negligible when fresh epinephrine is
added to a plain solution.
Chloroprocaine plus 1 mL of sodium bicarbonate for 30 mL of solution raises the
pH to 6.8. Adding 1 mL of sodium bicarbonate per 10 mL of lidocaine or mepivacaine
raises the pH of the solution to 7.2 and adding 0.1 mL of bicarbonate per 10 mL of
bupivacaine raises the pH of the solution to 6.4 (from Mulroy’s Regional Anesthesia, 3rd
edition, 2002).
Carbonation
Another approach to shortening onset time has been the use of carbonated local
anesthetic solutions. These solutions contain large amounts of carbon dioxide, which
readily diffuses into the axoplasm of the nerve, lowering the pH and favoring the
formation of the cationic active form of the local anesthetic inside the cell. Carbonated
solutions are not available in the United States.
20 | P a g e
action. According to Neal (Reg Anesth Pain Med 2003;28:124-134) adding 5 mcg/mL
(1:200,000 dilution) prolongs the duration of lidocaine for peripheral nerve blocks from
186 min to 264 min. Adding only 2.5 mcg/mL (1:400,000 dilution) prolongs the block to
240 min (almost the same prolongation), without apparent effect on nerve blood flow.
Patients with micro angiopathy (e.g., diabetics), who could be at increase risk for neural
ischemia secondary to vasoconstriction, potentially could benefit from the use of more
diluted epinephrine. Adding only 1:400,000 epinephrine to local anesthetic solutions for
nerve blocks has become the standard in our practice, in both diabetics and non-diabetics
patients.
Intrathecal epinephrine does not lead to cord ischemia, because it does not
decrease spinal cord blood flow, although it decreases epidural blood flow (Kosody R, et
al. Can Anaesth Soc J; 31: 503-8, 1984).
In fact spinal cord ischemia due to epinephrine is “improbable because the cord vessels
are autoregulated and show very minimal response to endogenous or exogenous
vasoactive agents” (Neal JM In: Regional Anesthesia, The Requisites. Elsevier Mosby,
Philadelphia 2004, pp 25-31)
Although epinephrine-containing local anesthetics are usually contraindicated in
areas of terminal circulation (e.g., digits) this recommendation is not based on hard
evidence. Anecdotal use of epinephrine-containing solutions in digits is cited in the
literature. Lalonde et al published a multicenter study including 3,110 consecutive cases
of use of epinephrine in the fingers and hand from 2002-2004. The authors (surgeons)
defined “low dose” epinephrine as 1:100,000 and they reported no instance “of digital
tissue loss” (J Hand Surg 2005; 30:1061-67). At this time we do not recommend this
practice.
Dilution/concentration issues
Opioids
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populations like the elderly and debilitated. Neuraxial morphine is also associated
with higher incidence (40-50%) of nausea and vomiting than systemic opioids,
more pruritus (60-80%, 20% of it severe), and delayed voiding. It is not suitable
for outpatients.
Short-acting opioids, such as fentanyl and sufentanil, when added to spinal
anesthetics can also intensify the block, and prolong the duration of anesthesia,
beyond the duration of local anesthetics. Respiratory depression with these agents
is rare and usually early (within 4 h). Sufentanil spinal can be used in doses of
2.5-10 mcg. Fentanyl spinal is used in doses of 10-25 mcg and 25-150 mcg
epidural. Onset occurs at 5-15 min, peak effect at 10-20 min and duration of 1-3
h. Hypotension, pruritus, nausea and vomiting are some common side effects.
Clonidine
22 | P a g e
anesthesia by 50%, compared to placebo, after a mid-humeral block, without prolonging
motor effect. Because the prolongation was observed only in the nerves that received
clonidine they postulated that the effect must be peripheral and not central through
absorption.
Dexmedetomidine
It is a more selective alpha-2 agonist agent with an alpha-2:alpha-1 receptor ratio
of 1,600:1, seven times greater than that of clonidine. Its elimination half-life is only 2 h
compared to more than 8 h for clonidine. Dexmedetomidine may offer extended
analgesia with lesser side effects. Currently it is approved only for sedation in the ICU.
Neostigmine
It is an acetylcholinesterase inhibitor that prevents the breakdown of acetylcholine
promoting its accumulation. Acetylcholine is an endogenous spinal neurotransmitter that
induces analgesia. Neostigmine does not cause neural blockade nor have any action on
opioid receptors.
Spencer Liu et al in 1999 (Anesthesiology 1999; 90:710-717) studied the effects
of different doses of neostigmine added to bupivacaine spinal. They reported that 50 mcg
of neostigmine increased sensory and motor anesthesia, but also delayed discharge time
and was accompanied by 67% nausea and up to 50% vomiting. Lower doses did not show
analgesic effect, but still had significant rates of side effects (nausea and vomiting).
Hyaluronidase
It breaks down collagen bonds potentially facilitating the spread of local
anesthetic through tissue planes. However, the evidence shows that at least in the epidural
space it can decrease the quality of anesthesia. Its use seems limited to retrobulbar blocks.
Dextran
Dextran and other high-molecular-weight compounds have been advocated to
increase the duration of local anesthetics. The evidence is lacking.
23 | P a g e
four times faster than tetracaine. However, even tetracaine has a metabolic half-life of
only 2.5-3.0 min (Tetzlatt JE. In: Ambulatory Anesthesia Perioperative Analgesia. New
York, McGraw-Hill, 2005, p 193).
In individuals with atypical plasma pseudocholinesterase the half-life of these
drugs is prolonged and potentially could lead to plasma accumulation. Cerebrospinal
fluid does not contain esterase enzymes, so if an ester is used for spinal anesthesia (e.g.,
tetracaine) its termination of action depends on blood absorption.
The hydrolysis of all ester local anesthetics leads to the formation of para-
aminobenzoic acid (PABA), which is associated with a low potential for allergic
reactions. Allergic reactions may also develop from the use of multiple dose vials of
amide local anesthetics that contain methylparaben (PABA derivative) as a preservative.
As opposed to other ester type anesthetics, cocaine is partially metabolized in the
liver and partially excreted unchanged in the urine.
They are transported into the liver before their biotransformation. The two major
factors controlling the clearance of amide local anesthetics by the liver are hepatic blood
flow and hepatic function.
The metabolism of local anesthetics as well as that of many other drugs occurs in
the liver by the cytochrome P-450 enzyme system. Because of the liver large metabolic
capacity it is unlikely that drug interaction would affect the metabolism of local
anesthetics. The rate of metabolism is agent specific (prilocaine > lidocaine >
mepivacaine > ropivacaine > bupivacaine).
The metabolism of amide local anesthetics is relatively fast, although slower than
esters. Elimination half-life for lidocaine is 1.5-2 h. Drugs such as general anesthetics,
norepinephrine, cimetidine, propranolol and calcium channel blockers can decrease
hepatic blood flow and potentially increase the elimination half-life of amides. Similarly,
decreases in hepatic function caused by a lowering of body temperature, immaturity of
the hepatic enzyme system in the fetus, or liver damage (e.g., cirrhosis) can lead to
decreased rate of hepatic metabolism of the amides. Renal clearance of unchanged local
anesthetic is a minor route of elimination (e.g., lidocaine is only 3% to 5% recovered
unchanged in the urine of adults, while bupivacaine is 10% to 16%).
24 | P a g e
30 min. A number of 20 is related to the homozygous atypical enzyme and the effect of
succinylcholine could be expected to last up to 6 h (incidence 1:3,300).
LOCAL ANESTHETIC TOXICITY
1. Total dose
2. Net absorption, which depends on: vasoactivity of the drug, site vascularity and
use of a vasoconstrictor
3. Metabolism and elimination of the drug from the circulation
25 | P a g e
Tumescent (diluted) anesthesia for liposuction
The following are accepted plasma levels of selected local anesthetics, above
which systemic effects are expected in humans:
Lidocaine 5 mcg/mL; mepivacaine 5 mcg/mL; bupivacaine 1.5 mcg/mL;
ropivacaine 4 mcg/mL
26 | P a g e
Management of systemic toxicity
The best treatment for toxic reactions is prevention. When local anesthetic-
induced seizures occur, hypoxia, hypercarbia and acidosis develop rapidly. ABC
(Airway, Breathing and Circulation) is the mainstay of treatment. Administration of O2
by mask, or ventilation support by bag and mask, is often all that is necessary to treat
seizures. If seizures interfere with ventilation, benzodiazepines, propofol or thiopental
can be used. The use of succinylcholine effectively facilitates ventilation and, by
abolishing muscular activity, decreases the severity of acidosis. However neuronal
seizure activity is not inhibited and therefore, cerebral metabolism and oxygen
requirements remain increased.
In an interesting study by Mayr et al, out of Innsbruck, Austria (Anesth Analg
2004; 98: 1426-3), the authors induced cardiac arrest in 28 pigs by administering 5 mg/kg
of 0.5% bupivacaine and stopping ventilation until asystole occurred. CPR was initiated
after 1 min of cardiac arrest. After 2 min the animals received every 5 min either
epinephrine alone; vasopressin alone; epinephrine plus vasopressin or placebo IV. In the
vasopressin/epinephrine group all pigs survived and in the placebo group all pigs died. In
the vasopressin alone 5 of 7 survived and in the epinephrine group 4 of 7 survived. This
is in line with current ACLS recommendations of using one single dose of 40U of
vasopressin IV before using epinephrine.
Little information is available regarding the treatment of local anesthetic
cardiovascular toxicity in humans. Animal data suggest:
1. Vasopressin 40 U, IV, single dose, one time only followed by, if needed,
high doses of epinephrine (1 mg IV every 3-5 minutes) to support heart
rate and blood pressure.
2. Atropine may be useful for bradycardia.
3. DC cardioversion is often successful.
4. Ventricular arrhythmias are probably better treated with amiodarone than
with lidocaine. Amiodarone is used as for ACLS, 150 mg over 10 min,
followed by 1 mg/min for 6 hrs then 0.5 mg/min. Supplementary infusion
of 150 mg as necessary up to 2 g. For pulseless VT or VF, initial
administration is 300 mg rapid infusion in 20-30 mL of saline or dextrose
in water.
27 | P a g e
bolus of 20% lipid emulsion (such as intralipid), followed by an infusion of 0.25 mL/kg/
min for 10 min, and the continuation of basic life support. The bolus can be repeated
every 5 min, up to three times as needed. The maximum dose of 20% lipid emulsion is
not known, but the authors suggest that more than 8 mL/kg would not likely be needed,
nor successful, if lower doses do not work. This protocol will deliver a significant volume
load to the patient. The paper was accompanied by an editorial by Groban and
Butterworth from Wake Forest, in Winston-Salem, North Carolina. They believe that the
most likely mechanism of action of lipid emulsion is that “in some way the lipid is
serving to more rapidly remove LA molecules from whatever binding site serves to
produce the cardiovascular depression that has come to be known as bupivacaine
toxicity”.
ACLS protocols must be followed with prompt defibrillation and use of pressors
like vasopressin followed by epinephrine, to support coronary perfusion if necessary.
Amiodarone should be favored over lidocaine to treat arrhythmias and initiate the lipid
emulsion at the “earliest sign of severe local anesthetic-induced cardiac toxicity.
In 2006 Rosenblatt et al (Anesthesiology 2006; 105: 217-8) published a case
report of successful use of 20% lipid emulsion (Intralipid, Baxter Pharmaceuticals) on a
58-year old male who developed a cardiac arrest, presumably linked to bupivacaine after
an interscalene block. They described that after 20 min of cardiac compressions and with
the patient in asystole, 100 mL of intralipid IV was given resulting in an apparent
“immediate” return of patient’s rhythm. This dose is higher than the recommended 1 mL/
kg. A continuous infusion of intralipid was given at 0.5 mL/kg/min for 2 h. The patient
was extubated 2.5 after hours after the episode, without any apparent neurological
sequelae. In an accompanying editorial, Weinberg suggested having 20% lipid emulsion
available in all sites where local anesthetics are used.
Also in 2006, soon after Rosenblatt’s report, Litz et al reported a case of
successful use of intralipid after ropivacaine-induced asystole. More recently, in March
2008, McCutchen and Gerancher reported a case of ventricular tachycardia treated with
150 mg of amiodarone, 10 mL of 20% intralipid and a synchronized countershock of 120
J, after which there was a prompt return to normal sinus rhythm. The authors speculate
that the use of intralipid might have prevented the patient from going into cardiac arrest.
In summary:
1. Evidence is accumulating on the beneficial effect of a 20% lipid emulsion to treat
bupivacaine-related cardiac toxicity.
2. Propofol has the same vehicle than intralipid, but only half the concentration
(10%). Giving propofol probably will not provide enough lipids, but instead it
will produce a negative inotropic effect due to the presence of the active
ingredient di-isopropylphenol (anesthetic action), exacerbating cardiac
depression. Therefore, propofol is not indicated to treat local anesthetic-induced
cardiac toxicity.
Maximum dose
28 | P a g e
recommended doses”. However the traditional recommendations are based on
extrapolation from animal data that do not necessarily apply to clinical practice.
According to Rosenberg et al, the common recommendations for maximum doses, as
suggested by the literature, “are not evidence based” (Reg Anesth Pain Med 2004; 29:
564-575), and according to Milroy have proven to be “poor approximation of safety”
(Reg Anesth Pain Med 2005; 30: 513-515).
It is known that peak plasma levels do not correlate with patient size or body
weight. Many practitioners have called to review these guidelines to better reflect the
reality of clinical practice. The American Society of Regional Anesthesia convened a
“Conference in Local Anesthetic Toxicity” with a panel of experts in 2001, to discuss the
subject. Many papers related to that conference have been published. In a review article
by Rosenberg et al (just cited) the authors argue that the safe doses instead should be
block specific and related to patient’s age (e.g., epidural), organ dysfunction (especially
for repeated doses) and whether the patient is pregnant. They suggest also adding
epinephrine 2.5 to 5 mcg/mL, when not contraindicated.
The fact is that most of the systemic toxicity occurs with unintentional direct
intravascular injection (Mather et al, Reg Anesth Pain Med 2005; 30: 553-566).
Methemoglobinemia
Allergy
True allergy (type I or IgE mediated) to local anesthetics is rare and presents
within minutes after the exposure. It is relatively more frequent with esters, which are
metabolized to para-amino-benzoic acid (PABA). PABA is frequently used in the
pharmaceutical and cosmetic industries. Allergy to amide local anesthetics is exceedingly
29 | P a g e
rare. There is no cross allergy between esters and amides. However use of methylparaben
as a preservative in multidose vials can elicit allergy in patients allergic to PABA.
Delayed hypersensitivity reactions (type IV) are T-cell mediated and present 24 to
48 h after exposure. There are few cases in the literature of delayed hypersensitivity to
lidocaine, but recent reports suggest it may be more frequent than previously reported.
The North American Contact Dermatitis Group found that 0.7 % of patients who were
patch tested in 2001-02 demonstrated delayed allergy to lidocaine (ASRA News,
February 2006).
Drug interactions
1. Procaine:
Type: ester
Pka: 8.9
Protein biding: 5%
Characteristics: intermediate onset, low potency, short duration. Very short half-
life (20 sec).
Other: it provides a short-duration spinal (potential benefit on outpatients).
2. 2-Chloroprocaine:
Type: ester
Pka: 9.3
Protein binding: negligible
Characteristics: very fast onset, despite high pka (ability to use higher
concentrations could be the reason). Short duration (it has 30 minutes 2-segment
regression in epidural). Very short half-life (30 sec).
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Other: The original preparation contained sodium metabisulfite as a preservative.
It was associated with serious neurological deficits when a large injection,
planned for epidural, ended intrathecally. A second preservative, ethylenediamine
tetra-acetic acid (EDTA) was associated with severe muscle spasm after epidural
in ambulatory patients. EDTA chelates ionized calcium and this side effect may
be secondary to action on paraspinal muscles.
The present solution is prepared without preservatives, and no back spasms have
been reported.
3. Tetracaine:
Type: ester
Pka: 8.6
Protein binding: 85%
Characteristics: slow onset, high potency, long duration. Short plasma half-life
(2.5 to 4 min).
Other: early experience with this product at high doses resulted in CNS toxicity,
giving it a bad reputation, mostly undeserved. We still use it occasionally in our
practice, as lyophilized crystals dissolved in liquid mepivacaine for a final
concentration of 0.2% tetracaine. It prolongs duration of surgical anesthesia in
peripheral nerve blocks to 4-6 h. Tetracaine also is the drug that gets the longest
prolongation from adding epinephrine to spinal anesthesia (up to 60% in the
lumbar dermatomes).
4. Cocaine:
Type: ester
Pka: 8.6
Protein binding: ?
Characteristics: slow onset, short duration. Elimination half life 60-90 min.
Urinary excretion of unchanged cocaine is usually less than 1%, but it can be up
to 9% especially in acid urine. At the end of 4 hours, most of the drug is
eliminated from the plasma. Cocaine metabolites (benzoylecgonine and ecgonine)
may be present in the urine for 24-36 hours, but some metabolites may be
identified for up to 144 h after administration (Ellenhom and Barceloux, 1988).
Other: It produces vasoconstriction, while most of the LA with the exception of
ropivacaine, produce some degree of vasodilation. It interferes with the reuptake
of cathecolamines, resulting in hypertension, tachycardia, arrhythmias and
myocardial ischemia. It is used mainly for topical anesthesia of the nose. Doses
below 100 mg (2.5 mL) are usually safe.
Cocaine can potentiate cathecolamine-induced arrhythmias by halothane,
theophylline or antidepressants. Cocaine can induce coronary vasospasm and
potential myocardial ischemia, without the need for coronary artery disease.
Mixtures of lidocaine and phenylephrine are safer alternatives.
5. Benzocaine:
Type: ester
Pka 3.5
31 | P a g e
Characteristics: slow onset, short duration and the only LA with a secondary
amine structure that limits its ability to pass through membranes (topical use
only).
Other: Doses higher than 300 mg can induce methemoglobinemia.
6. Lidocaine:
Type: amide
Pka: 7.8
Protein binding: 65%
Characteristics: intermediate onset and duration, elimination half-life 45-60 min.
Other: it is versatile (topical, infiltration, IV regional, neuraxial, antiarrhythmic)
and widely used. Spinal use is associated with around 30% of TNS, especially
with lithotomy position, knee arthroscopy and obesity. Lowering the
concentration does not eliminate the problem with doses larger than 40 mg. Doses
of 25-40 mg highly reduce the incidence of TNS.
7. Mepivacaine:
Type: amide
Pka: 7.6
Protein binding: 75%
Characteristics: intermediate onset and duration. Elimination half-life is 2-3 h in
adults and 8-9 h in neonates.
Other: It seems to produce less vasodilation than lidocaine. It has been used in
spinal anesthesia. It has lower (but not zero) incidence of TNS.
It is the agent we most commonly use for peripheral nerve blocks. A 1.5% of
plain solution provides a short onset and dense surgical anesthesia lasting 2-3 h
(3-4 h with 1:400,000 epinephrine). Prolonged postoperative analgesia, as with all
other LA, is negligible after single-shot blocks.
8. Bupivacaine:
Type: amide
Pka: 8.1
Protein binding: 95%
Characteristics: high potency, slow onset, long duration. Elimination half-life
3-3.5 h in adults and around 8 h in neonates.
Other: lower concentrations (0.25% and less) produce analgesia with increased
motor sparing (desirable in outpatients and obstetrics). Commercial bupivacaine is
a 50:50 racemic mixture of the R and S enantiomers. Cardiac arrest associated
with bupivacaine is difficult to treat possibly due to its high protein binding and
high lipid solubility (please see toxicity).
9. Ropivacaine:
Type: amide
Pka: 8.2
Protein binding: 94%
32 | P a g e
Characteristics: onset and duration similar to bupivacaine, with slight lesser
potency. Elimination half-life 1-3 h in adults.
Like bupivacaine, it is chemically related to mepivacaine, but as opposed to most
local anesthetics, it is supplied as the pure S enantiomer of the drug. The S
enantiomer is associated with less cardiac toxicity, intermediate between that of
lidocaine and bupivacaine.
Other: It is a weak vasoconstrictor (only one other than cocaine). At lower
concentrations (less than 0.5%) it may show a greater selectivity for sensory than
motor blockade than bupivacaine.
10. Levobupivacaine:
Type: amide
Pka: 8.1
Protein binding: 97%
Characteristics: S enantiomer of bupivacaine, very similar to ropivacaine.
Not available at this time in the US.
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References
1. Lou L, Sabar R, Kaye A: Local Anesthetics, In: Raj P (ed), Textbook of Regional
Anesthesia. New York, Churchill Livingstone, 2002, pp 177-213
2. Brown DL, Fink R: The History of Neural Blockade and Pain Management, In:
Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3rd edition. Philadelphia,
Lippincott-Raven, 1998, pp 3-32
3. Strichartz GR: Neural Physiology and Local Anesthetic Action, In: Cousins MJ,
Bridenbaugh PO (eds), Neural Blockade, 3rd edition. Philadelphia, Lippincott-
Raven, 1998, pp 35-54
4. Tucker GT, Mather LE: Properties, Absorpton, and Disposition of Local
Anesthetic Agents, In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3rd
edition. Philadelphia, Lippincott-Raven, 1998, pp 55-95
5. Covino BG, Wildsmith JAW: Clinical Pharmacology of Local Anesthetic Agents,
In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3rd edition.
Philadelphia, Lippincott-Raven, 1998, pp 97-128
6. Morgan GE, Mikhail MS, Murray MJ: Clinical Anesthesiology, 4th edition. New
York, McGraw-Hill, 2006, pp 263-288
7. Mulroy MF: Regional Anesthesia, 3rd edition. Philadelphia, Lippincott Williams
& Wilkins, 2002, pp 1-63
8. Liu SS, Joseph RS: Local Anesthetics, In: Barash PG, Cullen BF, Stoelting RK
(eds), Clinical Anesthesia. Philadelphia, Lippincott Williams & Wilkins, 2006, pp
453-471
9. DiFazio CA, Carron H, Grosslight KR, et al. Comparison of ph-adjusted lidocaine
solutions for epidural anesthesia. Anesth Analg 1986; 65: 760-64
10. Hilgier M. Alkalinization of bupivacaine for brachial plexus block. Reg Anesth
1985;10: 59-61
11. Booker PD, Taylor C, Saba G. Perioperative changes in α1-acid glycoprotein
concentrations in infants undergoing major surgery. Br J Anaesth 1996; 76:
365-368
12. Stoelting RK: Pharmacology and Physiology in Anesthetic Practice, 3rd edition.
Philadelphia, Lippincott-Raven, 1999, pp158-181
13. Tetzlaff JE: Local anesthetics and adjuvants for ambulatory anesthesia. In: Steele
SM, Nielsen KC, Klein SM (eds), Ambulatory Anesthesia Perioperative
Analgesia. New York, McGraw-Hill, 2005, pp 193-205
14. Weinberg GL et al. Lipid emulsion infusion rescues dogs from bupivacaine-
induced cardiac toxicity. Reg Anesth Pain Med 2003; 28:198-202
15. Mayr VD, Raedler C, Wenzel V, et al. A comparison of epinephrine and
vasopressin in a porcine model of cardiac arrest after rapid intravenous injection
of bupivacaine. Anesth Analg 2004; 98:1426-3
16. Neal JM. Effects of epinephrine in local anesthetics on the central and peripheral
nervous systems: Neurotoxicity and neural blood flow. Reg Anesth Pain Med
2003; 28:124-134
17. Rosenberg PH, Veering VT, Urmey WF. Maximum recommended doses of local
anesthetics: A multifactorial concept. Reg Anesth Pain Med 2004; 29: 564-575.
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18. Mulroy MF. Local anesthetics: Helpful science, but don’t forget the basic clinical
steps (editorial). Reg Anesth Pain Med 2005; 30: 513-515.
19. Mather LE, Copeland SE, Ladd LA. Acute toxicity of local anesthetics:
Underlying pharmacokinetic and pharmacodynamic concepts (A review article).
Reg Anesth Pain Med 2005; 30: 553-566
20. Horlocker TT. One hundred years later, I can still make your heart stop and your
legs weak: the relationship between regional anesthesia and local anesthetic
toxicity. Reg Anesth Pain Med 2002; 27(6): 543-4
21. Mulroy MF. Systemic toxicity and cardiotoxicity from local anesthetics:
Incidence and preventative measures (editorial). Reg Anesth Pain Med 2002;
27(6): 556-61
22. Horlocker TT, Wedel DJ. Local, anesthetic toxicity-Does product labeling reflect
actual risk? Reg Anesth Pain Med 2002; 27(6): 562-567
23. Weinberg GL. Current concepts in resuscitation of patients with local anesthetic
cardiac toxicity. Reg Anesth Pain Med 2002; 27(6): 568-575
24. Myer Leonard. Carl Koller: Mankind’s greatest benefactor? The story of local
anesthesia. J Dent Res 1998; 77:535-8
25. De Jong R. Tumescent anesthesia: lidocaine dosing dichotomy. Int J Cosmetic
Surg 2002; 4: 3-7
26. Nordstrom H, Stange K. Plasma lidocaine levels and risks after liposuction with
tumescent anaesthesia. Acta Anaesthesiol Scand 2005; 49: 1487-1490
27. Rosenblatt MA, Abel M, Fischer GW, et al. Successful use of a 20% lipid
emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac
arrest. Anesthesiology 2006; 105:217-8
28. Litz RJ, Popp M, Stehr SN, et al. Succesful resuscitation of a patient with
ropivacaine-induced asystole after axillary plexus block using lipid infusion.
Anaesthesia 2006; 61: 800-801
29. Rodriguez J, Quintela O, Lopez-Rivadulla M, et al. High doses of mepivacaine
for brachial plexus block in patients with end-stage chronic renal failure. A pilot
study. Eur J Anaesthesiol 2001; 18: 171-176
30. Kamibayashi T, Maze M. Clinical uses of α2-adrenergic agonists. Anesthesiology
2000; 93:1345-9
31. Tanoubi I, Vialles N, Cuvillon P, et al. Systemic toxicity with mepivacaine
following axillary block in a patient with terminal kidney failure. Ann Fr Anesth
Reanim 2006; 25:33-5
32. McCutchen T, Gerancher JC. Early Intralipid Therapy May Have Prevented
Bupivacaine-Associated Cardiac Arrest. Reg Anesth Pain Med 2008; 33: 178-180
35 | P a g e
CHAPTER 3
NEURAXIAL ANESTHESIA
36 | P a g e
SPINAL ANESTHESIA
It is one of the easiest and most reliable techniques of regional anesthesia. The
very small doses of local anesthetics used to produce spinal anesthesia are devoid of
direct systemic effects.
In 1885 James Corning, an American neurologist, was the first person to use
cocaine intrathecally to treat some neurological conditions. Augustus Bier, a German
surgeon, was the first person to use intrathecal cocaine to produce surgical anesthesia. In
a classic paper published in 1899, he described the failed attempt, by his assistant
Hildebrandt, to perform a spinal anesthesia on him, and his successful spinal on
Hildebrandt. Both of them became the first patients suffering from post dural puncture
headaches.
Anatomy
The spinal canal has a protective sheath composed of three layers. From the
outside to the inside they are: duramater, arachnoid and piamater. The potential space
between the dura and arachnoid is called subdural space. The cerebrospinal fluid (CSF)
flows between the arachnoid and piamater in the space called subarachnoid space.
The spinal cord begins cranially at the foramen magnum, as a continuation of the
medulla oblongata. It terminates caudally at the conus medullaris, which in the adult
corresponds to the level of the lower border of L1, and in the young child to the upper
border of L3. From this end, a prolongation of the piamater called the filum terminale
attaches the spinal cord to the coccyx. The dural sac itself ends at the level of the second
sacral vertebra.
The spinal cord is composed of a core of gray matter surrounded by white matter.
The gray matter on cross section has an H shape, with ventral (motor) and dorsal
(sensory) horns. The white matter is described as having anterior, lateral and posterior
white columns.
There are 31 pairs of spinal nerves; each one being formed by two roots, a ventral
or motor root and a dorsal or sensory root. The dorsal root has the dorsal root ganglion.
Because the spinal cord of an adult is shorter than the vertebral column, the spinal nerves
descend a variable distance in the spinal canal before exiting through the intervertebral
foramen. The most distal lumbar and sacral nerves travel the longest distance inside the
spinal canal, forming what is known as the cauda equina. As the spinal nerve pierces the
dural sac, it draws with it a dural sleeve. The spinal nerves exit through the intervebral
foramen, formed between two vertebrae. There are 8 cervical nerves. The first cervical
nerve exits through the occipital bone and C1, the 8 th cervical nerve exits between C7 and
T1. Distal to T1 each spinal nerve exits below the corresponding vertebra.
The vertebral column has a series of curvatures in the anteroposterior plane. The
cervical and lumbar curvatures have an anterior convexity (lordosis) and the thoracic and
sacral have posterior convexity (xiphosis). These curvatures play a role in the spread of
the local anesthetic solution, as we will review later.
The blood supply to the spinal cord comes from one anterior spinal artery and two
posterior spinal arteries. These arteries anastomose to form longitudinal vessels,
reinforced by segmental arteries that enter the vertebral canal trough the intervertebral
37 | P a g e
foramina. The anterior two thirds of the spinal cord are supplied by the anterior spinal
artery reinforced in the neck by branches of the vertebral artery.
In the thoracic region the anterior spinal artery receives only a few radicular
arteries from the aorta. In the lumbar region a large branch called radicularis magna or
artery of Adamkiewicz, reinforces the anterior spinal artery. It arises 78% of the times on
the left side, and typically enters the spinal canal through a single intervertebral foramen
between T8 and L3. This important branch is at risk of damage during retroperitoneal
dissections (e.g., surgery on the distal aorta), which could lead to ischemia of the spinal
cord. A case of transient paraplegia after neurolytic celiac plexus block on a pancreatic
cancer patient was reported in 1995 by Wong and Brown. The proposed mechanism was
reversible arterial spasm post injection of ethanol solution.
The needle used to perform a diagnostic spinal tap or a spinal anesthesia needs to
cross the skin, subcutaneous tissue, supraspinous ligament, interspinous ligament,
ligamentum flavum, duramater and arachnoid, before reaching the subarachnoid space
and CSF. The space between the ligamentum flavum and duramater is the epidural space.
Cerebrospinal fluid
It is primarily formed in the choroids plexus of the cerebral ventricles. The CSF
flows from the lateral ventricles to the third and fourth ventricles, and from there to the
cisterna magna. It flows then around the brain and spinal cord, within the subarachnoid
space. The CSF is absorbed into the venous system of the brain by the villi in the
arachnoid membrane. CSF is formed and reabsorved at a rate of 0.3-0.4 mL/min.
The CSF volume in the brain is between 100-150 mL. The volume of CSF below
T12, where most of the spinal anesthetics are performed is, according to Hogan and
collaborators, widely variable among individuals, ranging from 28-80 mL. CSF volume is
decreased with increased abdominal pressure, like the one accompanying pregnancy and
obesity. Therefore, increased abdominal pressure could potentially lead to higher spread
of a neuraxial blockade.
CSF Serum
Sodium (mEq/L) 141 140
Potassium (mEq/L) 2.9 4.6
Calcium (mEq/L) 2.5 5.0
Magnesium (mEq/L) 2.4 1.7
Chloride (mEq/L) 124 101
Bicarbonate (mEq/L) 21 23
Glucose mg/100mL) 61 92
Protein (mg/100mL) 28 7000
pH 7.31 7.41
Osmolality (mOsm/kg H2O) 289 289
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Site of action
The nerve root is the main site of action for both spinal and epidural anesthesia. In
spinal anesthesia the concentration of local anesthetic in CSF is thought to have minimal
effect on the spinal cord itself.
Indications
Abdominal and lower extremity procedures are the most common. It has been
used for lumbar spine surgery. Saddle blocks are frequently used for rectal surgery.
Baricity
It is the result of dividing density of the local anesthetic solution by that of the
CSF. The density of CSF has a mean value of 1.0003. If the baricity is 1.0 it is by
definition isobaric; if greater than 1 it is hyperbaric and if less than 1 it is hypobaric.
1. Hypobaric solutions
Tetracaine is the local anesthetic most frequently used for hypobaric spinal
anesthesia. Solutions of 0.1% to 0.33% tetracaine in water are reliably hypobaric
in all patients. The most common uses of hypobaric solutions are for rectal
procedures in jackknife position and for hip surgery injecting in lateral position
with the surgical side up.
2. Isobaric solutions
Tetracaine and plain bupivacaine diluted with CSF make good isobaric solutions.
These solutions stay very close to the point of injection.
3. Hyperbaric solutions
The easiest, safest and most widely used way of providing spinal anesthesia. The
solution is rendered hyperbaric by adding glucose. Gravity and patient’s position
determines the spread. In supine position L3 and T6 are the highest points of the
spine and subsequently they become the limits for spread.
1. Major factors
• Baricity acting together with gravity
• Position of patient (except isobaric solutions)
• Dosage, rather than volume or concentration
Baricity is the main factor that determines local anesthetic spread in the
subarachnoid space. It obviously works in conjunction with gravity and patient position.
When plain local anesthetics are used, total dose is more important than injected volume
or concentration. Van Zundert et al reported in 1996, that a 70 mg dose of plain
subarachnoid lidocaine produced the same quality of spinal block over a wide range of
concentrations and volumes. Sheskey et al in 1983 demonstrated similar sensory levels
with 10 mg of plain bupivacaine, at different concentrations and volumes. However,
doses of 15-20 mg of plain bupivacaine produced higher sensory levels of spinal (T2-T4
39 | P a g e
level) than 10 mg (T5-T8 level). When hyperbaric bupivacaine or tetracaine solutions are
used, similar levels of spinal blocks are obtained at different doses, when the
concentration is maintained constant. In the case of hyperbaric bupivacaine, it seems that
this applies as long as the dose is higher than 7.5 mg. Above this dose the level is
determined by baricity acting along with the curvatures of the spine, patient position, and
gravity. In general, the higher the spread the shorter the duration of the sensory blockade,
because the concentration of the drug decreases from the point of injection.
2. Minor factors
• Level of injection
• Increased abdominal pressure (obesity and pregnancy)
• Patient height (only at extremes)
• Coughing
• Direction of needle bevel can affect spread of isobaric preparations. The bevel
should be directed toward the desired region.
3. No effect
• Addition of vasoconstrictors
• Barbotage (aspirating and injecting technique to produce CSF turbulence)
• Age
• Gender
Techniques
Sitting, midline approach
Sitting position is commonly used for neuraxial blocks. It may be the preferred
position in patients whose midline may be difficult to determine, like obese patients. The
position of the iliac crest is frequently used to determine the L4-L5 interspace. However,
accumulation of adipose tissue around the patient mid section, could lead to a higher-
than-desired level for needle placement.
The Closed Claims Project shows cases of spinal cord injury by the spinal needle,
in which the level of needle placement was grossly underestimated. I suggest instead
using the upper end of the intergluteal sulcus to determine the position of the sacral
hiatus. In adults the L5-S1 interspace is around 10 cm (4 inches) cephalad to this point
(height of the sacrum). This measurement in adults should always be distal to the
termination of the spinal cord at L1.
Using a hyperbaric solution in the sitting position, and leaving the patient in that
position for at least 5 minutes, produces a saddle block. However, up to 20 minutes is
necessary to wait, in the desired position, to achieve any appreciable “saddle” or
“lateralized” distribution blockade.
Lateral position
It is the position of choice in many institutions. The patient lies on his/her side. It
is more comfortable for the patient and decreases the risk for accidental fall and
vasovagal problems. The technique otherwise is similar to sitting position
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Paramedian approach
In some elderly patients, with calcified ligaments, it is difficult to advance the thin
spinal needle through the midline. The lateral approach is a good alternative in those
cases. The spinous process is identified and the point of entrance is marked about 2 cm
paramedian. The needle is directed slightly medial and cephalad.
Taylor Approach
Usually the L5-S1 interspace is the larger. A spinal technique through it is known
as Taylor approach. The entrance point is 1 cm medial and 1 cm caudal to the posterior
superior iliac spine directing the needle cephalad and toward the midline.
Anesthesia duration
The local anesthetic used and the rate at which it is removed from the
subarachnoid space determines duration. Elimination is entirely dependent on vascular
absorption and does not involve metabolism of local anesthetics within the subarachnoid
space. Absorption occurs in the subarachnoid space itself and in the epidural space (local
anesthetics cross the dura both ways).
1. Hypotension
It is the most frequent seen side effect. It is mainly the result of venous pooling
with decreased cardiac output secondary to sympathetic blockade. There is also a
small component of arteriolar dilation. However systemic blood pressure does not
decrease proportionally because of compensatory vasoconstriction, especially in
the upper extremities with intact sympathetic innervation. Even with total
sympathetic blockade with spinal anesthesia the decrease in systemic vascular
resistance is < 15%. This is because arterioles retain intrinsic tone and do not
dilate maximally.
The extent of decrease in BP is dependent on the extent of sympathetic blockade,
intravascular volume, and cardiovascular status. Preloading the patient with
250-500 mL, while frequently used, is unsupported by the evidence.
A mild vasopressor like ephedrine in 5-10 mg increments and fluid are all that is
usually necessary to treat hypotension. Ephedrine is the drug of choice because it
produces vasoconstriction and increased cardiac output.
Phenylephrine is a good second choice especially if tachycardia is present. It
causes vasoconstriction, but it could decrease the cardiac output.
Trendelenburg position can alleviate the venous pooling, but may produce an
even higher spinal level. Flexion of the operating table with legs and back up is a
good compromise.
2. Bradycardia
When the sympathetic block reaches T2 level the cardioacelerator fibers are
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blocked and the vagus action is unopposed. The extent to which hear rate
decreases in response to total sympathetic block during spinal usually is moderate
(10-15%). However severe bradycardia and asystole have been reported in
normal patients during otherwise uneventful spinal anesthesia. It can occur even
in the absence of hypotension and can occur after 30-45 minutes of spinal.
The Bezold-Jarisch reflex has been implicated. This reflex would be triggered by
decreased venous return to the heart producing a paradoxical hypervagal
response. Early recognition and treatment is essential. Ephedrine, atropine and
in some cases epinephrine are indicated along with fluid replacement. |
3. Total spinal
Spinal anesthetic that involves the cervical region. It is manifested by respiratory
arrest, bradycardia, hypotension and unconsciousness. The respiratory arrest most
likely is a manifestation of ischemia of the medullary respiratory center secondary
to intense hypotension and drop in cardiac output (complete sympathetic
blockade) severe enough to compromise cerebral circulation. Block of phrenic
nerve is not a likely cause. Management involves ABC with control of the airway,
use of vasopressors, atropine and fluid replacement as needed.
2. Hepatic
Hepatic blood flow decreases to the extent of hypotension to a degree similar than
after general anesthesia. Spinal anesthesia has not proven to be an advantage or
disadvantage in patients with liver disease. For intraabdominal surgery the
decrease in hepatic perfusion is mainly due to surgical manipulation.
3. Renal
Renal blood flow as cerebral blood flow is autoregulated through a wide range of
arterial pressure. In the absence of renal vasoconstriction renal blood flow does
not decrease until mean arterial pressure decreases below 50 mm Hg. Thus, in the
absence of severe hypotension, renal blood flow and urinary output remain
unaffected during spinal anesthesia. Loss of autonomic bladder control results in
urinary retention. This is more frequent in males.
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ACTH, cortisol, epinephrine, norepinephrine and vasopressin as well as activation
of the rennin-angiotensin-aldosterone system. However this effect seems to wear
off along with the spinal anesthesia, producing metabolic and hormonal responses
similar than after general anesthesia for the same operation.
5. Gastrointestinal
The small intestine contracts during spinal and sphincters relax due to unopposed
vagus nerve activity. The combination of contracted gut and complete relaxation
of abdominal muscle provide good surgical conditions.
1. Nausea
Frequent side effect due to imbalance of sympathetic and parasympathetic
visceral tone. Hypotension, bradycardia or hypoxia must be rule out.
Antiemetics like ondansetron or droperidol are usually effective.
• Pencil point needles less than or equal to 22 gauge and cut-bevel needles
less than or equal to 27 gauge produce an incidence of PDPH of
approximately 1%.
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• Continuous spinal with 20 gauge catheters is not likely to produce PDPH
in an older patient population.
• Obstetric patients undergoing spinal anesthesia with small pencil point
needles show a 3-4% rate of post dural puncture headache. Conservative
treatment involves bed rest, IV or oral fluids, acetaminophen and NSAIDs.
Hydration and caffeine stimulates production of CSF.
• Epidural blood patch with 15-20 mL of autologous blood, injected at the
same original puncture level or one space below, is a very effective
treatment. The effect can be immediate or be delayed by a few hours. A
single blood patch is about 90% effective.
The cause for TNS is not well understood and could represent a mild and
reversible form of neuropathy. Many possible causes have been postulated: local
anesthetic toxicity, needle trauma, neural ischemia secondary to sciatic nerve
stretching, patient positioning, small gauge, pencil-point needles promoting local
anesthetic pooling, muscle spasm, early mobilization, etc. Because of the low
incidence of TNS after bupivacaine spinal, we could be reasonably sure than TNS
is not the result of the subarachnoid block per se, the needle or the position for it.
Even though neurotoxicity is frequently mentioned as possible cause for TNS,
a case can be made against it. Cauda equina syndrome (CES) is known to result
from local anesthetic toxicity; however the factors that increase CES (e.g., higher
doses/concentration of local anesthetics and the addition of vasoconstrictors), do
not have an effect on TNS.
We know that TNS is mostly associated with lidocaine spinal, lithotomy
position, knee arthroscopy and ambulatory surgical status (obesity could be a
contributing factor) and that it is very rarely associated with bupivacaine spinal.
We also know that decreasing the concentration of lidocaine from 5% to 0.5%
does not decrease the incidence of TNS and that hyperosmolarity, hyperbaricity
and addition of glucose ARE NOT contributing factors.
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First line of treatment is reassurance, NSAIDs, comfortable positioning and
heating pad. A second line of treatment can include narcotics and muscle
relaxants like cyclobenzaprine. Trigger point injections have been used with
reported success.
Eliminating lidocaine from subarachnoid block probably is not warranted at
this point. However do not use it for ambulatory surgery in lithotomy position or
knee arthroscopy (high risk). On the other hand, the incidence of TNS after
inguinal hernia with lidocaine spinal is only 8%, after C-section is 0-8% and after
tubal ligation is 3%, similar to non-pregnant patients undergoing surgery in the
supine position. Bupivacaine, even in small doses, increases discharge time.
Perhaps the combination of small doses of bupivacaine plus narcotics is the best
possible approach.
6. Hearing loss
Transient minor hearing loss has been described after spinal anesthesia. The risk
seems larger with larger-gauge needles and it might be the result of temporary
decrease in CSF pressure with traction of intracranial nerves.
The problem is mild but well documented with audiometry. It resolves on its own.
7. Infection
Abscess or meningitis is rare. The development of meningitis after lumbar
puncture in bacteremic patients is a concern. Animal models suggest that
perioperative use of antibiotics eliminates this risk. Lumbar puncture in patients
infected with HIV is controversial. Neuraxial techniques including blood patch
have been performed on these patients without apparent problems. The risk has to
be evaluated on an individual basis.
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Spinal anesthesia in the outpatient setting
A few years ago spinal anesthesia was favored for same day surgery patients.
However, widely available, poorly-soluble general anesthetic agents and LMA have
decreased its use. Home readiness involves short duration of action and, in many
institutions, ability to void. Duration is a function of the agent and dose used. The spread
of the agent dictates the duration at a given dermatome. It is likely that the more
segments blocked by a given dose (more spread) the shorter the duration at any given
segment. Hyperbaric solutions and isobaric solutions injected rapidly with the bevel
turned caudad concentrates around the sacral roots and can delay sensory motor recovery
and the ability to void. On a milligram basis, isobaric preparations injected rapidly with
the bevel facing cephalad are more likely to improve home readiness and voiding.
Procaine and very small doses of bupivacaine and other anesthetics plus narcotics have
been used in the outpatient setting with variable success.
Intrathecal adjuncts
1. Epinephrine
It prolongs duration, but also prolongs the recovery time and voiding time. Thus it
should not be used in the ambulatory setting.
2. Fentanyl
The lipophilic synthetic opioids appear to improve the quality of the block
without prolonging recovery (as opposed to epinephrine). Ben-David et al in
1997, showed that 5 mg of hyperbaric bupivacaine was inadequate in 27% of
cases of spinal for knee arthroscopy. Adding 10 ucg of fentanyl reduced the
failure rate to zero.
Fentanyl produces pruritus in about 50% of the patients. Serotonin inhibitors (like
ondansetron) are being used to treat this side effect too. Respiratory effects are
unlikely with doses below 25 mcg.
3. Morphine
The use of hydrophilic intrathecal narcotics is accompanied by a longer lasting
analgesia, but also by a higher rate of complications. Among them are: delay
respiratory depression (4-6 hrs after the injected dose), increased nausea and
vomiting, pruritus and delayed voiding.
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EPIDURAL ANESTHESIA
It is technically more difficult to perform than spinal and because larger doses of
local anesthetics are used it has the potential for systemic toxicity. On the other hand, it
offers a greater degree of flexibility in the extent and duration of anesthesia.
Anatomy
The spinal epidural space extends from the foramen magnum to the end of the
dural sac at the level of S2. It is bounded anteriorly by the vertebral bodies and
posteriorly by the laminae and ligamentum flavum. The epidural space outlines the spinal
canal immediately superficial to the dura. In the cervical region the epidural space is
smaller and it is wider in the lumbar area. A volume of local anesthetic about 10 times
larger is required to produce lumbar epidural anesthesia than for equivalent subarachnoid
blockade. Smaller volumes are sufficient for the thoracic space. The epidural space is
filled with connective tissue, fat and veins, which can become enlarged during
pregnancy. The spinal nerves travel through this space surrounded by a sheath of dura.
47 | P a g e
Techniques
Lumbar epidural
It is the most common site for epidural anesthesia. The midline or paramedian
approach can be used. A block below the termination of the spinal cord at L1 should be
safer. An accidental dural puncture (“wet tap”) could result in spinal cord damage at
higher levels.
Thoracic epidural
It is technically more challenging and has a greater risk for spinal cord injury. It is
rarely used as the primary anesthetic. Many people prefer the paramedian approach in the
thoracic level, because of the extreme obliquity of the thoracic spinous processes.
Epidural needles
The Tuohy needle is the most commonly used. A typical needle is 17-18 gauge,
3.5 inches long. It has a blunt bevel with a gentle curve of 15-30° at the tip. The blunt tip
helps push the dura away, “tenting” it, after the ligamentum flavum has been pierced.
Epidural catheters
They provide the means for continuous infusion. Usually they are 19-20 gauge in
size. The needle bevel is directed in the desired direction (not a guarantee for catheter
final location) and the catheter is advanced 2-6 cm. A short insertion increases the chance
for accidental dislodgement. The farther in, the greater the chance of unilateral epidural
and other complications (bloody tap, catheter knotting). Four to five cm is a good
compromise.
Test dose
It is important because of the large doses of LA injected into the epidural space.
The classic test dose is 3 mL of 1.5% lidocaine (45 mg) with 1:200,000 of epinephrine
(15 mcg). The 45 mg of lidocaine, if intrathecal, should produce spinal anesthesia. The 15
mcg of epinephrine, if intravascular, should produce at least a 20% increase in heart rate
within 30 sec or 30 beats between 20-40 sec (Barash’s, 5th edition, 2006). In patients who
are beta blocked the heart rate increase may not happen and an increase in systolic
pressure of 20 mmHg or more may be more reliable (Barash’s 5 th edition, 2006). The use
of epinephrine as a test dose in obstetrics is controversial. Some suggest instead the use
of only 30 mg of lidocaine or 5 mg of bupivacaine.
Termination of action
It is related to type of drug and degree of spread. It is commonly described as the
time it takes to a two-segment regression of sensory blockade. The approximate time for
two-segment regression (sensory) for chloroprocaine is 50-70 minutes, for lidocaine is
90-150 minutes and for bupivacaine is 200-260 minutes.
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References
1. Snell R: Clinical Anatomy for Medical Students, 5th edition. Boston, Little,
Brown and Company, 1995
2. Bernards CM: Epidural and Spinal Anesthesia, In: Barash PJ, Cullen BF,
Stoelting RK, Clinical Anesthesia, 5th edition. Philadelphia, Lippincott Williams
& Wilkins, 2006, pp 691-717
3. Mulroy MF: Regional Anesthesia, 3rd edition. Philadelphia, Lippincott Williams
& Wilkins, 2002, pp 65-118
4. Wong G, Brown D. Transient paraplegia following alcohol celiac plexus block.
Reg Anesth 1995; 20: 352-355
5. Hogan QH. Magnetic resonance imaging of cerebrospinal fluid volume and the
influence of body habitus and abdominal pressure. Anesthesiology 1996; 84;
1341-1349
6. Bridenbaugh PO, Greene NM, Brull SJ, Spinal (Subarachnoid) Neural
Blockade, In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3rd edition.
Philadelphia, Lippincott-Raven, 1998, pp 203-241
7. Cousins MJ, Veering BT: Epidural Neural Blockade, In: Cousins MJ,
Bridenbaugh PO (eds), Neural Blockade, 3rd edition. Philadelphia, Lippincott-
Raven, 1998, pp 243-320
8. Salinas FV: Pharmacology of Drugs Used for Spinal and Epidural Anesthesia
and Analgesia, In: Wong CA (ed), Spinal and Epidural Anesthesia. New York,
McGraw-Hill, 2007, pp 75-109
9. Sheskey MC, Rocco AG, Bizzarri-Schmid M, et al. A dose-response study of
bupivacaine for spinal anesthesia. Anesth Analg 1983; 62: 931-935
10. Van Zundert AAJ, Grouls RJE, Korsten HHM, et al. Spinal anesthesia: Volume
or concentration-What matters? Reg Anesth 1996; 21: 112-118
11. Giroux CL, Wescott DJ. Stature estimation based on dimensions of the bony
pelvis and proximal femur. J Forensic Sci, 2008; 53: 65-68
12. Reina MA, de Leon-Casasola OA, Lopez A, et al. An in vitro study of dural
lesions produced by 25-gauge Quincke and Whitacre needles evaluated by
scanning electron microscope. Reg Anesth Pain Med 2000; 25: 393-402
13. Swisher JL. Spinal Anesthesia: Past and Present. In Problems in Anesthesia,
2000:12; 141-147
14. Ben-David B, Solomon E, Levin H, et al. Intrathecal fentanyl with small-dose
dilute bupivacaine: Better anesthesia without prolonging recovery. Anesth
Analg 1997: 85; 560-565
15. Pollock JE. Transient neurological symptoms: etiology, risk factors, and
management. Reg Anesth Pain Med 2002:27; 581-86
16. Morgan GE, Mikhail MS, Murray MJ: Clinical Anesthesiology, 4th edition. New
York, McGraw-Hill, 2006, pp 289-323
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CHAPTER 4
REGIONAL ANESTHESIA
AND ANTICOAGULATION
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Regional Anesthesia in the anticoagulated patient
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The following is a summary of the 2002 ASRA guidelines adapted with
permission from Neal JM: Neural Blockade and Anticoagulation. In: Regional
Anesthesia, The Requisites in Anesthesiology. Rathmell J, Neal J, Viscomi C (eds).
Philadelphia, Elsevier Mosby, 2004
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more fibrin-selective and have less effect on plasminogen. While the plasma half-
life of thrombolytic drugs is only hours, it can take days for the thrombolytic
effect to resolve; fibrinogen and plasminogen are maximally depressed at 5 hours
after this therapy and remain significantly depressed at 27 hours.
Contraindications to thrombolytic therapy include surgery or puncture of non-
compressible vessels within 10 days.
Recommendation:
• Patients on fibrinolytic and thrombolytic drugs should not receive spinal
or epidural procedures. Data are not available to recommend a precise
number of days. Ten days has been the usual recommendation.
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• Closely monitor patients postoperatively for signs and symptoms of spinal
hematomas.
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• Factor IX: 24 hr
• Factor X: 25 to 60 hr
• Factor 2: 50 to 80 hr
Factor activity level of 40% for each factor is adequate for normal hemostasis.
The PT and INR are most sensitive to the activities of factors VII and X and are
relatively insensitive to factor II.
Because factor VII has a short half-life prolongation of PT and INR may occur in
24 to 36 hr. Prolongation of the INR (More than 1.2) occurs when factor VII is
down to 55% of baseline, while an INR of 1.5 is associated with factor VII
activity of 40%. Thus an INR of more than 1.5 should be associated with normal
hemostasis.
Upon discontinuation of warfarin factor VII activity will rapidly increase and the
INR will decrease. However factor II and X recover much more slowly, thus
hemostasis may not be adequate even though the INR is 1.4 or less. Adequate
levels of all vitamin K-dependent factors are typically present when the INR is
less than 1.2.
In emergency situations the effect of warfarin can be reversed by vitamin K
injection and/or transfusion of fresh frozen plasma.
Recommendation:
• Do not perform neuraxial blocks on patients who have been on chronic
warfarin therapy.
• Caution should be exercised when patients have had their warfarin
discontinued prior to surgery. Ideally 4 or 5 days should elapse and PT
and INR should be measured prior to any neuraxial block. Remember
that early after warfarin discontinuation the PT/INR reflects
predominantly factor VII levels while the rest of factors activity is still
inadequate. Wait until PT and INR are normal.
• Concurrent use of medications that affect other components of the clotting
mechanism may increase the risk of bleeding and do so without affecting
PT/INR (aspirin and other NSAIDs, ticlopidine and clopidogrel).
• Patients receiving one initial dose more than 24 hr prior to block should
have PT/INR checked before proceeding.
• As thromboprophylaxis with warfarin is initiated with a catheter in place
during low dose warfarin therapy, PT/INR should be checked daily and
before catheter removal. The INR prior to removal should be less than 1.5.
• Continue neurological exams at least 24 hr after removal.
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mechanisms, while COX-2 mediates pain and inflammation (no effect on
platelets). Platelet function is affected for the life of the platelet following aspirin;
other nonsteroidals (naproxen, ibuprofen) have a short-term effect (3 days).
- COX-2 inhibitors like celecoxib (Celebrex) and rofecoxib (Vioxx) are anti-
inflammatory agents that affect COX-2 an enzyme not present in platelets, and
thus do not cause platelet dysfunction.
- The thienopyridine derivatives have antiplatelet effect from inhibition of
ADP-induced platelet aggregation. These agents are used in the prevention of
cerebrovascular thromboembolic events. Labeling recommends, “if a patient is to
undergo elective surgery, and an antiplatelet effect is not desired, clopidogrel
should be discontinued 7 days and ticlopidine 10-14 days prior to surgery.”
- Platelet GP IIb/IIIa receptor antagonists inhibit platelet aggregation by
interfering with platelet-fibrinogen and platelet-von Willebrand factor binding.
Time to normal platelet aggregation ranges from 8 hr (eptifibatide, tirofiban) to 24
to 48 hr (abciximab). Labeling precautions recommend that puncture of non-
compressible sites and “epidural” be avoided.
Recommendation:
• Difficult to generalize because these drugs have different effects
• There is no accepted test to guide antiplatelet therapy.
• NSAIDs: their use alone does not seem to create a level of risk that will
interfere with the performance of neuroaxial blocks.
At this time there is no specific concern as to the timing of single-shot or
catheter techniques or the timing of catheter removal in conjunction with
NSAIDs.
• Thyenopyridine derivatives: risk unknown. Follow labeling precautions:
clopidogrel (Plavix) 7days and ticlopidine (Ticlid) 14 days.
• GP IIb/IIIa antagonists: risk unknown. Follow label precautions: 48 hr for
abciximab and 4-8 hr for eptifibatide and tirofiban
• The concurrent use of other medications affecting clotting may increase
the risk of bleeding complications.
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• Mandatory discontinuation or cancellation of surgery is not supported by
available data.
• Concurrent use of other medications affecting clotting may increase the
risk of bleeding.
• No specific concern about timing of neuraxial catheter removal.
New antithrombotic drugs which target various steps in the hemostatic system, are
continually under development. The most extensively studied are antagonists of specific
platelet receptors and direct thrombin inhibitors. Many of these agents have prolonged
half-lives and are difficult to reverse without administration of blood components.
Thrombin inhibitors
Fondaparinux
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References
1. Neal JM: Neural Blockade and Anticoagulation. In: Regional Anesthesia, The
Requisites in Anesthesiology. Rathmell J, Neal J, Viscomi C (eds). Philadelphia,
Elsevier Mosby, 2004, pp 151-156
2. Bergqvist D, Wu CL, Neal JM. Anticoagulation and Neuraxial Regional
Anesthesia: Perspectives. [Editorial] Reg Anesth Pain Med 2003; 28: 163-166
3. Horlocker tt, Wedel DJ, Benzon H, et al. Regional anesthesia in the
anticoagulated patient: Defining the risks (The Second ASRA Consensus
Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med,
2003; 28: 172-197
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CHAPTER 5
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Peripheral Nerve Blocks
There are many ways to ascertain the correct placement of a needle with respect to a
nerve. A good knowledge of the anatomy makes things easier and safer. The methods are:
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mixed nerve, a painless muscle twitch is produced. The intensity of the response
is inversely proportional to the needle tip-nerve distance (actually to the square
root of it). A visible response at lower currents (less than 0.5 mA), suggests close
proximity between the needle tip and the target nerve. There is a good amount of
clinical evidence to suggest that a current of 0.5 mA or less, capable of eliciting a
visible response, is a reliable indicator of critical proximity. However, evidence is
lacking as to what exactly that distance is, and as to whether the distance is
different for different nerves. In general it is thought that 1 mA of current will
produce depolarization of a motor nerve at a distance of about 1 cm (10 mm).
Nowadays nerve stimulator techniques are widely practiced around the
world. Since they do not necessarily rely on patient cooperation, they are
sometimes used in unconscious or heavily sedated patients. We do not encourage
this practice, as it can lead to complications that a conscious patient could perhaps
help prevent (e.g., intraneural injection). With modern nerve stimulators the
practitioner can adjust the pulse intensity (magnitude of the current) in mA; the
pulse frequency (amount of pulses per second) in Hz (1 or 2) and the pulse
width (duration of the pulse) in milliseconds (ms). The pulse duration most
suitable for stimulating motor fibers in a mixed nerve is 0.1 ms (100 microsec).
Characteristics of ultrasound
The human ear can hear sounds between 20 and 20,000 Hz (cycles per
second) or 20 KHz. Ultrasounds waves travel at a higher frequency than the
highest frequency detectable by the human ear. Ultrasound waves used in
medicine usually are in the 1 to 20 MHz range (1 MHz = 1 million Hz). High
frequency waves are shorter and good for superficial structures. Ultrasound
waves travel easily through fluids and soft tissue, but have problems traveling
through bone and air. Ultrasound is better reflected at the transition between two
different types of tissues like soft tissue-air, bone-air and soft tissue-bone.
The ultrasound is delivered from a small probe that contains a transducer.
The transducer converts electrical signals into ultrasound waves. The transducer
detects the reflected waves and converts them back into electrical signals, which
are eventually the source of the image we see on the screen. Therefore, the
transducer delivers ultrasound for part of the time and for part of the time it
“listens” for the returned waves. Some of the wave sounds pass through tissues,
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while others get reflected back into the transducer. The distance is calculated as a
function of the time it takes for the wave to return. Tissues with high density like
bones, reflect most of the waves and produce a bright image. These tissues are
known as hyperechoic. The hypoechoic structures are soft tissue structures with
different degrees of echo.
The more perpendicular the probe is to the structure being searched, (e.g.,
nerve), the better the image obtained, because more bouncing sound waves can be
detected by the transducer. This is also true when trying to visualize the needle.
Changes as small as 10 degrees from the perpendicular, can distort the
echogenicity of a nerve, by reducing the amount of waves returning to the
transducer.
The easiest way to identify a peripheral nerve is on a transverse scan, also
called “short axis view”. The needle, on the other hand, can be advanced with the
“out-of-plane” approach, crossing the ultrasound beam perpendicularly. The
needle becomes practically invisible as its cross section is one more of the
thousands of dots that form the ultrasound image. With the “in-plane” approach
the needle is advanced parallel to the probe. Depending on its depth and angle of
insertion the whole needle can be visualized. With either approach the needle is
aimed to the nerve surroundings.
Scanning superficial structures, like the brachial plexus, requires high
frequency probes (10-15 MHz) that provide good resolution, but limited
penetration (3-4 cm). For deeper structures like the brachial plexus in the
infraclavicular region or sciatic nerve in the buttocks, lower frequencies (4-7
MHz) are needed. Deep scanning of intra abdominal organs requires frequencies
of 3-5 MHz.
Standard needles have a tip angle of around 14 degrees and are known as “sharp’
needles. It is frequently recommended to perform regional block with short-bevel needles
with an angle of 30 to 45 degrees. This recommendation comes from studies by Selander
et al who demonstrated more neural damage in isolated sciatic nerves when sharp needles
were used. The damage with sharp needles was also more extensive when the orientation
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of the sharp bevel was perpendicular to the fibers. With short bevel needles, the damage
was less frequent as the fibers were pushed away by the advancing needle.
This concept has been challenged by Rice et al. In fact it may be more difficult to
penetrate a nerve fascicle with a short-bevel needle than with a sharp needle, but should it
occur, the lesions are more severe.
Nerve injury
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A preexisting neurological injury should always be documented. It is important to
realize that nerve damage can occur perioperatively for a reason other than regional
anesthesia. Nerves can be injured during surgery by direct trauma, use of retractors and
tourniquets and by improper positioning. Nerves can also be damaged postoperatively by
a tight cast or splint, wound hematoma or surgical edema.
Use of epinephrine
The symptoms can appear within 24 h after the injury, but sometimes they do not
present until days or weeks after the offending procedure took place. The degree of
symptoms is usually related to the severity of the injury. The symptoms can be mild, like
tingling and numbness that usually disappear within weeks to more rarely severe cases of
neuropathic pain and motor involvement that can last months and even years.
In order to minimize the risk of neurologic injury after regional anesthesia several
factors are important, including patient selection and type of surgeon. A meticulous nerve
block technique, avoiding direct trauma to the nerve and an appropriate selection of local
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anesthetic concentration, is also important. The role of vasoconstrictors, especially low
dose (1:400,000), on clinical development of neural ischemia, has not been elucidated.
When a neuropathy develops in the postoperative period, a prompt evaluation is
necessary and a multidisciplinary approach, with participation of neurology, radiology,
and surgery, is recommended. A detailed history must be obtained including the timing
and nature of symptoms. A physical exam should look for any signs or hematoma or
infection. A neurological exam by a neurologist is also crucial.
Electrophysiological testing
Use of tourniquet
Use of crude compression devices to control surgical bleeding from the
extremities, can be traced back, according to Bailey, to ancient Rome. The term
“tourniquet” was apparently first used by Petit in France in 1718, to describe a
mechanical screw-like contraption that he introduced to provide surgical hemostasis.
Lister in 1864, was the first surgeon, who used the tourniquet to produce a bloodless
surgical field. Modern tourniquet devices have a microprocessor, use an air pump and are
able to accurately and safely maintain the desired pressure. A fail-safe mechanism
protects from pressure ever exceeding 500 mmHg.
Tourniquet time: Recommended tourniquet time varies, but the most commonly
accepted limit is 2 hours. This recommendation is based on a work by Wilgis, published
in 1971 in which he demonstrated more acidosis after 2 hours of use. Surgeons should be
made aware of 2-hour tourniquet time and tourniquet should be deflated at that time,
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unless the surgeon is at a crucial time of the operation and requests more time. This
communication with the surgical team needs to be documented in the chart.
Despite the widely accepted 2 hour limit, Klenerman, as cited by Bailey, has shown
minimal muscle damage under electron microscopy, with tourniquet times not exceeding
3 hours.
Some people advocate deflating the tourniquet at 1.5h for 5-15 minutes and then re
inflate it for an additional 1.5 h.
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burning, cramping or heaviness. The burning and aching sensations, characteristics of
ischemia, are believed to be conducted by unmyelinated fibers (MacIver and Tanelian,
1992), while the sharp pain, usually a small component of tourniquet pain, is transmitted
by A-delta fibers. MacIver and Tanelian proposed that C fiber activation by ischemia-
induced alterations are responsible for tourniquet pain. They studied in an in-vitro model
the effects of ischemic alterations (i.e., hypoxia, hypoglycemia, lactic acid, and decreased
ph), on A-delta and C pain fibers. They showed that hypoxia and hypoglycemia induced
under ischemia, increased C fiber tonic action potential activity, but did not affect A-delta
fibers. Increased lactate and decreased pH did not alter the discharge frequency of C
fibers in this model. The activation of C fibers by ischemia products seems crucial in
tourniquet pain. Whether these C fibers eventually enter the spinal cord at a level above
the somatic nerve block is debatable.
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References
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18. Martin G, Breslin D, Stevens T: Anesthesia for Orthopedic Surgery, In:
Longnecker DE, Brown DL, Newman MF, Zapol WM (eds), Anesthesiology.
New York, McGraw Hill, 2008, pp 1541-1557
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CHAPTER 6
UPPER EXTREMITY NERVE BLOCKS
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UPPER EXTREMITY BLOCKS
The brachial plexus is most commonly formed by five roots originating from the
ventral divisions of spinal nerves C5 through T1. The roots of the plexus are located in
the cervical paravertebral space, between the anterior and middle scalene muscles.
Besides understanding its origins, it is also important to understand the plexus in terms of
the relative surface area occupied by its components at different levels of its trajectory.
As shown in figure 6.1 each root of the plexus emerges from an intervertebral foramen.
The C5 root appears between cervical vertebrae 4 and 5, while the T1 root emerges
between thoracic vertebrae 1 and 2.
The distance from C5 to T1 roots is large and irreducible, and it is equal to the
height of four vertebrae. This fact helps to explain why during an interscalene block,
usually performed at C5 or C6 level, dermatomes derived from C8-T1 are frequently
missed. C8-T1 roots are simply too far from the site of injection. Another important and
frequently ignored reason is the expansive, pulsatile effect of the subclavian artery over
the C8 and T1 roots, preventing the local anesthetic from reaching them.
When the five roots combine together to form three trunks, not only there is a
40% reduction in the number of nerve structures (from 5 to 3), but also the trunks become
physically contiguous. This is the point where the brachial plexus is reduced to its
smallest surface area. This area of high concentration of nerve structures helps to explain
the rapid onset and high success rate of the supraclavicular approach. This special
circumstance is only seen in the brachial plexus and has not parallel in the lower
extremity. The surface area of the plexus increases again when the trunks originate six
divisions and even further when the plexus ends up by giving off terminal branches in the
axilla.
The anterior scalene muscle originates in the anterior tubercles of the transverse
processes of C3 to C6 and inserts on the scalene tubercle of the upper surface of the first
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rib. The middle scalene muscle originates in the posterior tubercles of the transverse
processes of C2 to C7 and inserts on a large area of the upper surface of the first rib,
behind the subclavian groove.
The five roots converge toward each other to form three trunks -upper, middle and
lower-stacked one on top of the other, as they traverse the triangular interscalene space
formed between the anterior and middle scalene muscles. This space becomes wider in
the anteroposterior plane as the muscles approach their insertion on the first rib.
While the roots of the plexus are long, the trunks are almost as short (1-2 cm) as
they are wide, soon giving rise to a total of six divisions (three anterior and three
posterior), as they reach the clavicle. The area of the trunks corresponds to the point
where the brachial plexus is confined to its smallest surface area, three nerve structures,
closely related to one another. They carry the entire sensory, motor and sympathetic
innervation of the upper extremity, with the exception of a small area in the axilla and
upper middle arm, which is innervated by the intercostobrachial nerve, a branch of the
second intercostal nerve. This special arrangement is mandated by the narrow passage
between the clavicle and the first rib that the neurovascular bundle must negotiate before
getting into the axilla.
The brachial plexus enters the apex of the axilla lateral to the axillary artery,
which is the continuation of the subclavian artery. At this point the divisions rearrange
and mixed their fibers to form three cords, lateral, medial and posterior, named after their
relative position to the axillary artery. The cords travel caudally in close proximity to the
coracoid process, under the cover of the pectoralis minor muscle, which itself is covered
by the pectoralis major muscle. At about the level of the lateral border of the pectoralis
minor muscle the three cords give off their terminal branches. The posterior cord
originates the axillary and radial nerves; the medial cord originates part of the median
nerve, plus the ulnar, medial brachial and medial antebrachial cutaneous nerves. The
lateral cord originates the rest of median nerve and musculocutaneous nerve. Very often
the musculocutaneous nerve remains attached to the median nerve until reaching the
proximal arm.
Axillary nerve (C5-C6): gives an articular branch to the shoulder joint, motor innervation
to the deltoid and teres minor muscles and sensory innervation to part of deltoid and
scapular regions.
Radial nerve (C5-C6-C7-C8-T1): supplies the skin of the posterior and lateral arm down
to the elbow, the posterior forearm down to the wrist, lateral part of the dorsum of the
hand and the dorsal surface of the first three and one-half fingers proximal to the nail
beds. It also provides motor innervation to the triceps, anconeus, part of the brachialis,
brachioradialis, extensor carpi radialis and all the extensor muscles of the posterior
compartment of the forearm. Its injury produces a characteristic “wrist drop”.
Median nerve (C5-C6-C7-C8-T1): gives off no cutaneous or motor branches in the axilla
or the arm. In the forearm it provides motor innervation to the anterior compartment
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except the flexor carpi ulnaris and the medial half of the flexor digitorum profundus
(ulnar nerve). In the hand provides motor innervation to the thenar eminence and the first
two lumbricals. It provides the sensory innervation of the lateral half of the palm of the
hand and dorsum of first three and one-half fingers including the nail beds.
Ulnar nerve (C8-T1): like the median nerve, the ulnar nerve does not give off branches in
the axilla or the arm. Its motor component supplies the flexor carpi ulnaris and the medial
half of the flexor digitorum profundus. In the hand it provides the motor supply to all the
small muscles of the hand except the thenar eminence and first two lumbricals (median).
Its sensory branches supply the medial third of the dorsum and palmar sides of the hand
and dorsum of the 5th finger and dorsum of the medial side of 4th finger.
Medial brachial cutaneous nerve (T1): it is solely a sensory nerve. It supplies the skin of
the medial side of the arm. It is joined here by the intercostobrachial nerve, branch of the
second intercostal.
Medial antebrachial cutaneous nerve (T1): It is also a sensory nerve. It supplies the
medial side of the anterior forearm.
Pearls
• With the shoulder down the three trunks of the brachial plexus are located above
the clavicle, therefore during a supraclavicular block the needle should never
need to reach below the clavicle.
• For the most part the first intercostal space is located below the clavicle (with the
exception of the most posterior paravertebral part), therefore its penetration is
unlikely during a properly performed supraclavicular block.
• The needle should never cross medial to the parasagital plane of the anterior
scalene muscle because of risk of pneumothorax.
• The pulsatile effect of the subclavian artery exerted mainly against C8-T1 roots
and the lower trunk explains why the C8-T1 dermatome can be spared during a
supraclavicular block. To avoid this problem the injection needs to be performed
in the vicinity of the lower trunk, demonstrated by fingers twitch with a nerve
stimulator or by injecting behind the subclavian artery when using ultrasound).
• The SCM muscle inserts on the medial third of the clavicle, the trapezius muscle
on the lateral third of it, leaving the middle third for the neurovascular bundle.
These proportions are maintained regardless of patient’s size. Bigger muscle bulk
through exercise does not influence the size of the muscle insertion area.
• The brachial plexus crosses the clavicle at or near its midpoint. Because of the
direction of the brachial plexus from medial to lateral as it descends, the higher in
the supraclavicular area the more medial (closer to the SCM) the plexus is
located.
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INTERSCALENE BLOCK
Indications
Its main indication is anesthesia of the shoulder, lateral part of the clavicle and
proximal part of the humerus.
Main characteristics
This block is superficial and usually easy to perform. Characteristically it misses
the C8-T1 dermatome, which includes ulnar nerve, medial antebrachial cutaneous nerve
and medial brachial cutaneous nerve.
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Fig 6-3. Finding the interscalene
groove. The interscalene groove
is found behind the SCM at the
horizontal level of the cricoid
cartilage.
(On a model with permission).
A needle directed just medial has a bigger chance to enter the intervertebral
foramen and produce intravascular injection (vertebral artery) or penetrate the
subarachnoid and epidural spaces. This is a superficial block that should take place not
deeper than the projection of the clavicular head of the SCM. With that in mind further
penetration putting in risk the neuraxis are discouraged.
Any distal motor twitch as well as biceps, triceps or deltoid muscles are adequate.
A twitch of the abdomen signals phrenic nerve stimulation and it is evidence that the
needle is anterior to the anterior scalene. The needle should be withdrawn and redirected
posteriorly. A motor twitch of the trapezius muscle indicates stimulation of the spinal
accessory nerve and signals that the position of the needle is posterior to the brachial
plexus and needs to be repositioned anteriorly.
The injection of the local anesthesia is started slowly with frequent aspirations.
There is some confusion as to whether a shoulder twitch is acceptable. Anatomical and
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clinical evidence support accepting any twitches other than trapezius (please see:
Silverstein W et al. Interscalene block with a nerve stimulator: A deltoid motor response
is a satisfactory endpoint for successful block. Reg Anesth Pain Med 2000; 25:356-359
and accompanying editorial by William Urmey, same journal page 340-342).
Ultrasound technique
The area is best visualized by placing the probe obliquely across the anterior and
middle scalene muscles at the level of C5-C6. The SCM is identified as well as the great
vessels (common carotid and internal jugular). The internal jugular vein is easily
collapsible by the probe, which helps with its identification. Behind and somewhat lateral
to the SCM the anterior and middle scalene are usually easily visualized and the roots of
the plexus appear in between them with a characteristic honeycomb appearance. The
needle is advanced in plane with the probe, from lateral to medial, with a slight posterior
and caudal deviation, similar to Winnie’s approach. The needle is brought under direct
visualization into the proximity of C6 root. The spread of local anesthetic should show
the interscalene space expanding.
Clinical pearls
• Because of the position of the shoulder, so close to the head of the patient, the
anesthesiologist must carefully evaluate the patient and surgeon before deciding
to perform an interscalene block as the only anesthesia for the case. Rough
movements by the surgeon could scare the patient.
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• It must be remembered that most of these procedures are performed in positions
other than supine (e.g., beach chair, prone, lateral), therefore management of the
airway is a concern.
• Language barrier between patient and anesthesiologist is also a relative
contraindication for interscalene block as the sole anesthetic.
• This is a very superficial block. Care should be taken not to introduce the needle
more than 2 cm beyond the projection of the midpoint of the SCM muscle.
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SUPRACLAVICULAR BLOCK
Indications
This block is ideally suited for any surgery on the upper extremity that does not
involve the shoulder.
Main characteristics
This block is considered more difficult to learn than other upper extremity blocks
and historically has been associated with a higher risk of pneumothorax. The literature
cites pneumothorax rates between 0.5-6.1 percent. However with good anatomy and
meticulous technique we have been able to practically eliminate this risk.
A supraclavicular block is usually associated with a short onset and high success
rates. This is due to the compact arrangement of the plexus at this level. The location of
such large amount of innervation in such reduced area does not have a parallel in the
lower extremity, or anywhere else for that matter, qualifying the supraclavicular block as
the most successful plexus block in the whole body. Indeed it has been called the “spinal
of the upper extremity”.
Because of pneumothorax reports, the supraclavicular block started to lose its
appeal and by the 1960’s the axillary block started to become popular. A rational
approach should have dealt with the pneumothorax issue by finding reliable superficial
landmarks for the dome of the pleura. An anatomical approach that starts by determining
the pleura boundaries is the technique we perform and the reason for its safety and
reliability. This allows us to take advantage of such extraordinary block while limiting its
potential drawbacks. Our experience to late 2007 includes more than 3,500
supraclavicular techniques without any pneumothorax ever being demonstrated. A
common question posed to us is whether we perform routine chest X-rays after a
supraclavicular block. The fact is that we only do an X-ray when the clinical situation
calls for it (e.g., an unusually difficult technique). The literature predominantly shows
that when a pneumothorax has been found following a supraclavicular block, it has been
after the patient developed clinical symptoms and not during routine chest x-ray post
block. So our practice of performing selective chest X-rays, as needed, is comparable to
the common practice in the rest of the country.
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Albeit with several modifications, the supraclavicular block remained a popular
choice until the early 1960’s. Eventually, the combined effect of pneumothorax risk and
the introduction of the axillary approach by Accardo and Adriani in 1949, and especially
by Burnham in 1958, marked the beginning of the decline for one of the best regional
anesthesia techniques ever described.
The axillary approach introduced a good technique with its share of shortcomings
(e.g., smaller area of anesthesia than supraclavicular, tendency to produce “patchy”
blocks and lower overall success rate), but definitely devoid of pneumothorax risk. The
axillary block received a big push when in 1961 De Jong published an article in
Anesthesiology praising it. The paper was based on cadaver dissections and included the
now famous calculation of 42 mL as the volume needed to fill a cylinder 6 cm long, that
according to De Jong “should be sufficient to completely bathe all branches of the
brachial plexus”. Coincidentally (or not) the same journal carried a paper by Brand and
Papper out of New York, comparing axillary and supraclavicular techniques. This article
is the source of the 6.1% pneumothorax rate frequently quoted for supraclavicular block.
In retrospect these two articles could be considered the point at which the tide definitely
turned against the supraclavicular block making the axillary route the most common
approach to the brachial plexus in the United States and the rest of the world. With some
exceptions this is still true today.
Some authors also cite the perceived complexity of supraclavicular block as the
reason for not performing it more often. However the advantages of a supraclavicular
technique, namely its rapid onset, density, high success rate along with large area of
anesthesia are too good to ignore. These good characteristics are, according to David
Brown and colleagues, “unrivaled” by other techniques. In our practice the
supraclavicular approach is the cornerstone of upper extremity regional anesthesia.
Ultrasound has produced a resurgence in the interest to perform supraclavicular blocks
once again.
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The point at which the clavicular head of the SCM muscle inserts in the clavicle is
then identified as shown in fig 6-6. A parasagital (parallel to the midline) plane that
crosses this point determines an “unsafe” zone medial to it, where the risk of
pneumothorax is high and a lateral zone that is safer.
Because the trunks are short and run in a very steep direction caudally towards the
clavicle, there is a narrow “window of opportunity” to perform the block above the
clavicle. It must be performed at enough distance from the insertion of the clavicular
head to be away from the pleura, and close enough to this point to still reach the trunks,
before they disappear behind the clavicle. We call this distance “the safety margin”. In
adults we calculate this distance to be about 1 inch (2.5 cm), which corresponds to the
width of the author’s thumb. This distance is marked on the skin over the clavicle for
orientation, as shown in figure 6-7.
This is only an orientation point because the actual point of needle entrance is
determined by palpation of the most lateral elements of the plexus in the supraclavicular
area around the orientation point. At this level the brachial plexus is usually easily
palpable, either as a groove or some type of cord. This is usually called “interscalene
groove”, but the interscalene groove only exists high in the C5-C6 level.
The palpating finger is placed parallel to the clavicle and the point of needle
entrance is marked with a downward pointing arrow, as shown in figure 6-8 (upper lateral
arrow). Over the clavicle an upward pointing arrow is also drawn, as shown in figure 6-8
(lower lateral arrow). Both arrows together show the direction of the needle, parallel to
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the midline. The lower lateral arrow also marks the caudal limit for penetration of the
needle (as far caudal as we are willing to go), keeping it supraclavicular and away from
the first intercostal space.
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The reference to the midline is easy to ascertain and avoids the use of other
landmarks (e.g., nipple), which have enormous patient-to-patient location variability.
The needle is advanced caudally with a slight posterior angle. Because the trunks
are physically contiguous a twitch of the upper trunk (shoulder) is followed by middle
trunk (pectoralis, triceps, supination, pronation) and finally lower trunk (wrist and
fingers). The goal of the technique is to stimulate the fingers. Wrist flexion and extension
are acceptable responses, but supination or pronation or other more proximal twitches are
not.
If advancing the needle, after finding a proximal trunk, makes the twitch
disappear it means that the angle of the needle is not matching the orientation of the
trunks, and that the tip of the needle is wandering away from the trunks. The needle is
slowly withdrawn until the original twitch is once again visible, and then redirected either
posteriorly (most of the times) or anteriorly, but always parallel to the midline.
It is very important not to advance the needle more than 2 cm in the caudal
direction if no twitch is visible. In this case the situation is reassessed starting with the
nerve stimulator and its connections. As long as a twitch from the brachial plexus is being
elicited the needle can be safely advanced caudally without regard to depth.
Ultrasound technique
We also use the semi sitting position. A linear, high frequency probe, as for the
interscalene block, is used. We usually start scanning high in the neck at above C6 to
identify SCM, scalene muscles and great vessels. The probe is then advanced caudally
and placed just above the clavicle and almost parallel to it. The angle (tilting) is adjusted
to get a good cross section of the subclavian artery and the scalene muscles. The plexus,
either trunks or divisions, are visualized behind and proximal to the artery in a
characteristic honeycomb arrangement.
The needle is directed in plane from lateral to medial under the probe. The needle
should be inserted at 1-2 cm away from the probe to avoid a steep angle of insertion that
would make its visualization harder. The needle is directed toward the lower trunk,
behind the subclavian artery. The anesthetic solution should be seen surrounding the
plexus.
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Complications
Besides the common complications accompanying any block, the supraclavicular
technique can also be followed by Horner’s syndrome, hoarseness and phrenic nerve
palsy, but less frequently than after interscalene block. Neal et al in 1998 studied
diaphragmatic paralysis in 8 volunteers after supraclavicular block using ultrasound
(replicating what Urmey et al did in 1991 to demonstrate 100% of diaphragmatic
paralysis after interscalene block). They found an incidence of 50% of diaphragmatic
paralysis. No subject experienced changes in pulmonary function tests (PFT) values or
subjective symptoms of respiratory difficulty. This is our experience too.
Clinical pearls
• This is not a block for a practitioner that rarely performs peripheral nerve blocks.
The person interested in learning to perform it should first become familiar with
the anatomy of the supraclavicular area including the location of the dome of the
pleura. Using ultrasound makes the visualization of the pleura easier, but still
requires the operator to be familiar with the anatomy of the area.
• When using a nerve stimulator technique, the block should not be attempted
unless the insertion of the sternocleidomastoid in the clavicle is clearly
established. In fact this is a must especially for a person not experienced with the
technique. With time it becomes easier to ascertain the boundaries of the SCM.
• It helps to know that the neurovascular bundle crosses the clavicle under the
midpoint of it, so this should be kept in mind as a reliable reference.
• Due to the steep direction of the plexus from the neck to the axilla, the higher in
the neck (the further away from the clavicle) the more medial the plexus is. By the
same token, the further below the clavicle the more lateral to its midpoint the
plexus is.
• The needle should never be inserted more than 2 cm caudal if no twitch is elicited.
This warning applies to every patient regardless of weight.
• The injection should always be slow, alternated with frequent aspirations. This
technique provides time to recognize accidental intravascular injection in those
cases where blood is not aspirated. I also believe it helps to keep the needle from
moving backwards as a result of high speed flow at the tip of the needle.
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INFRACLAVICULAR BLOCK
Indications
This block is more suited for surgery distal to the elbow.
Main characteristics
The infraclavicular block is really an axillary block in which the needle enters the
axilla through its anterior wall (pectoralis muscles), instead of through its base. This fact
is usually unrecognized and infraclavicular block is presented as a block completely
different than axillary. It is a good place to place a catheter since it is less mobile than
neck and axilla. It also hurts more because is a deep block that requires the needle to go
through muscle. Patients should be adequately sedated.
It is widely recommended to obtain a distal twitch in the hand or wrist and to
avoid a biceps twitch (musculocutaneous nerve or lateral cord) or pronation of the
forearm (lateral cord). This is based on clinical experience. A bicepts twitch could be the
result of musculocutaneous nerve stimulation, outside the sheath, or from lateral cord
stimulation inside the sheath, and as such it is unreliable. It is theoretically possible that a
twitch from the posterior cord (elbow, wrist and or finger extension) could be best,
because the posterior cord is located at about the same distance from the other two, and
subjected to more pressure from surrounding structures, although it is more difficult to
get to it. Ultrasound, with visualization of the axillary artery, makes the injection
posterior to it easy.
Many infraclavicular techniques have been described. A simple technique is the
coracoid approach first described by Whiffler in the British Journal of Anaesthesia in
1981 and later redefined by MRI studies performed in 40 volunteers by Wilson, Brown et
al, and published in Regional Anesthesia in 1998.
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Nerve stimulator technique
The nerve stimulator is set to deliver a current of 0.9-1.0 mA at a frequency of 1
Hz and 0.1 ms of pulse duration. It is frequently necessary to use a 4” (10 cm) needle to
be able to reach the plexus.
The needle attached to the nerve stimulator is advanced in the anteroposterior
direction, perpendicular to the skin, as shown in figure 6-12.
Before entering in contact with the plexus the needle passes through the pectoralis
major and pectoralis minor muscles producing a visible local twitch. The brachial plexus
is found deep to them. If not response from the plexus is obtained the needle is redirected
caudal (most of the time) or cephalad, but maintaining the same parasagital plane without
medial or lateral deviation.
Ultrasound technique
Because the brachial plexus at this level is deep, being located under pectoralis
major and minor muscles, a lower frequency linear probe is usually used, in the range of
4-7 MHz. The probe is aligned almost perpendicular to the junction between the middle
and lateral thirds of the clavicle in the proximity of the coracoid process. This way a
cross section of the plexus and axillary vessels is obtained. The tilt is adjusted until a
clear view in cross section is obtained. The needle can be advanced in plane with the
probe from proximal to distal or vice versa. The best target, if a single injection is
desired, is the posterior cord behind the artery. Separate injections of the cords can be
done as needed.
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Complications
Pneumothorax can occur due to injury of the pleura through an intercostal space.
Muscle pain and hematomas, which can be large in size, are not uncommon.
Clinical pearls
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AXILLARY BLOCK
Indications
It is best suited for surgery distal to the elbow.
Main characteristics
The axillary block is not properly a plexus block, but rather a block of the
terminal branches of the brachial plexus. The distance between the different branches
plus the expanding wave of the axillary artery pulse are obstacles that the local anesthetic
must overcome to adequately reach the nerves. A single injection technique is an option,
but a second and even a third injection has shown to increase the success rate. If a single
injection is to be attempted, the epicenter of the injection if possible, has to coincide with
the specific nerve responsible for the sensory innervation of the surgical area. For
example, to deal with an extensor tendon injury of the thumb (radial nerve) the injection
should occur around the radial nerve. The same is true for lesions located in the ulnar and
median territories. If the surgical area involves more than one terminal nerve, the single
injection technique should be performed in the proximity of the radial level, because I
believe the solution diffuses more easily from back to front that vice versa. This may be
because of more resistance in the back of the plexus (muscles and scapula) than in front
(subcutaneous tissue). The anatomy lab also shows that better diffusion could be obtained
by placing a pillow under the elbow with the shoulder abducted slightly less than 90
degrees.
A point usually stressed in the literature is to perform the block as proximal in the
axilla as possible. This can be uncomfortable to the patient and challenging to the
anesthesiologist. The only perceived advantage would be to increase the chances of
blocking the musculocutaneous nerve before it leaves the plexus. This is never certain. A
better strategy is to block this nerve first before performing the block of the rest of
terminal branches.
Although some variability exists, usually the median nerve is superficial (anterior)
to the artery following its same direction, the ulnar nerve (and medial
brachial/antebrachial cutaneous) are medial and somewhat posterior to the artery, the
musculocutaneous nerve is lateral to the artery (and eventually under the biceps muscle)
and the radial nerve is posterior to the artery.
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Fig 6-13. The arm is abducted
about 80°, the elbow is elevated
slightly with a small pillow and
the axillary artery is marked.
(On a model with permission).
At some point under the biceps a motor twitch of the elbow in flexion is elicited.
The current is reduced to 0.5 mA and 5 mL of local anesthetic solution is slowly given.
The needle is then withdrawn and the nerve stimulator is set again to 0.8-0.9 mA. Using
the mark of the axillary artery on the skin as a reference, the needle is directed either
tangential to it (median), medial to it (ulnar and medial brachial/antebrachial) or posterior
to it (radial), as shown in figure 6-15.
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Ultrasound technique
The brachial plexus once again is superficial here so a linear, high frequency
(10-15 MHz) probe is used. The arm is abducted and a pillow is placed under the elbow,
as described for the nerve stimulator technique. The probe is placed across the
neurovascular bundle to get a cross section image of it. The median nerve is usually seen
superficial (anterior) to the artery. The ulnar nerve is medial and somewhat posterior, the
radial nerve is posterior. Distally in the axilla the radial nerve starts shifting more lateral,
but it still remains posterior to the artery. The musculocutaneous is lateral to the artery at
all times and it can be seen entering the coracobrachialis muscle. If a single injection is
planned it should be made in the proximity of the radial nerve. Individual injections of
terminal nerves can be done as needed.
Complications
Pneumothorax is virtually impossible to get from this location. Hematomas from
vascular puncture are more common and can be associated with nerve damage.
Pearls
• This is a block mainly indicted for surgery on the distal forearm, wrist and hand.
• It is not a good choice for elbow surgery.
• Tourniquet pain is an issue and not necessarily due to intercostobrachial nerve,
but mainly due to insufficient proximal anesthesia of the whole arm.
• The main injection should aim for the nerve most responsible for the sensory
innervation of the surgical site.
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References
1. Brown DL. Brachial plexus anesthesia: an analysis of options. Yale J Biol Med
1993; 66: 415-431
2. Franco CD, Vieira Z. 1,001 subclavian perivascular brachial plexus blocks:
success with a nerve stimulator. Reg Anesth Pain Med 2000; 25: 41-46
3. Franco CD. The subclavian perivascular block. Tech Reg Anesth Pain Med 1999;
3: 212-216
4. De Andres J, Sala-Blanch X. Peripheral nerve stimulation in the practice of
brachial plexus anesthesia: a review. Reg Anesth Pain Med 2001; 26: 478-483
5. Greenblatt Gm, Denson GS. Needle nerve stimulator-locator: nerve blocks with a
new instrument for locating nerves. Anesth Analg 1962; 41: 599-602
6. Hadzic A, Vloka J, Hadzic N, et al. Nerve stimulators used for peripheral nerve
blocks vary in their electrical characteristics. Anesthesiology 2003; 98: 969-974
7. Brown DL. Atlas of regional anesthesia. Philadelphia, PA: W.B. Saunders, 1992
8. Mulroy MF. Regional anesthesia: An illustrated procedural guide. 3rd edition.
Philadelphia, PA; Lippincott Williams & Wilkins 2002
9. Franco CD, Domashevich V, Voronov G, Rafizad A, Jelev T. The supraclavicular
block with a nerve stimulator: To decrease or not to decrease, that is the question.
Anesth Analg 2004; 98: 1167-1171
10. Neal JM, Hebl JR, Gerancher JC, Hogan QH. Brachial plexus anesthesia:
Essentials of our current understanding. Reg Anesth Pain Med 2002; 27: 402-428
11. Perlas A, Chan V: Ultrasound-assisted nerve blocks. In: Textbook of Regional
Anesthesia, Hadzic A (ed). New York, McGraw Hill, 2007, pp 663-672
12. Franco CD, et al. Gross anatomy of the brachial plexus sheath in human cadavers.
Reg Anesth Pain Med 2008; 33: 64-69
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CHAPTER 7
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LOWER EXTREMITY BLOCKS
The innervation of the lower extremity comes from the lumbar and sacral
plexuses. The different nerve elements of the lower extremity run more distant from each
other than those of the upper extremity, and they never get to be confined to a small
surface area like the trunks of the brachial plexus do. Therefore, no single peripheral
block technique is able to provide anesthesia of the whole lower extremity. This,
combined with the high success of neuraxial anesthesia, has contributed to make lower
extremity peripheral nerve blocks less popular than the techniques of the upper extremity.
The introduction of low molecular weight heparin, with its increased risk for
epidural hematoma in association with neuraxial blocks, has produced a renewed interest
in lower extremity nerve blocks.
Anatomy
Lateral femoral cutaneous nerve
It is an exclusively sensory nerve originating from the ventral rami of spinal
nerves L2-L3. It appears in the pelvis, lateral to the psoas muscle, caudal to the
ilioinguinal nerve. It runs anteriorly under the iliac fascia, parallel to the iliac crest. It
emerges from the pelvis, under the inguinal ligament, between the anterior superior and
anterior inferior iliac spines. It provides sensory innervation to the lateral thigh.
Femoral nerve
It is a motor and sensory nerve derived from the posterior divisions of the ventral
rami of spinal nerves L2-L3-L4. In the pelvis it is also located lateral to the psoas muscle,
in the cleavage between the psoas and the iliacus muscle. As it passes under the inguinal
ligament the nerve is superficial to the iliopsoas muscle. Approximately 3-4 cm below the
inguinal ligament, the femoral nerve divides into anterior and posterior divisions. The
anterior division has two sensory branches that supply the anteromedial thigh, and two
muscular branches that supply the sartorius and pectineus muscles. The posterior division
has one sensory branch, the saphenous nerve, and muscular branches to the quadriceps.
At it passes under the inguinal ligament the femoral nerve has the femoral artery medial
to it, followed by the femoral vein medial to the artery (VAN from medial to lateral). The
nerve is covered by the iliac fascia, which separates it from the main vessels, and more
superficially by the deep fascia of the thigh (fascia lata).
The muscular branch to the rectus femoris also supplies the hip joint while the
muscular branches to the three vasti muscles also supply the knee joint.
Obturator nerve
It is usually a mixed nerve (motor and sensory) derived from the anterior
divisions of the ventral rami of spinal nerves L2-L3-L4. It the pelvis is located on the
medial side of the psoas muscle. It runs along the lateral pelvis until it reaches the
obturator foramen, through which it enters the thigh. In the thigh the nerve divides into
anterior and posterior branches. The anterior division runs caudally, in front of the
obturator externus and the adductor brevis and behind the pectineus and adductor longus.
It gives innervation to the gracilis, adductor brevis and adductor longus, and sometimes
to the pectineus. It gives also articular branches to the hip joint. On occasions it supplies
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the skin of the medial side of the thigh. The posterior division pierces the obturator
externus and passes downwards, behind the adductor brevis and in front of the adductor
magnus. It supplies the obturator externus, the adductor magnus and the knee joint. The
anterior sensory branch can be frequently missing and in that case the medial thigh is also
supplied by the femoral nerve.
The highly variable distribution of the sensory branch of the obturator nerve has
contributed to the confusion about how much can be obtained from a single block
performed at the femoral level (“3-in-1” block).
Sciatic nerve
It is the largest nerve in the body. It originates from the ventral rami of spinal
nerves L4-L5, S1-S3. Part of the anterior ramus of L4 joins the anterior ramus of L5 to
originate the lumbosacral trunk, which together with the first three sacral roots form the
sciatic nerve. The nerve has two components, the tibial nerve (on its medial side), which
is derived from the anterior divisions of the ventral rami of L4-L5, S1-S3 and the
common peroneal nerve (on its lateral side), which is derived from the posterior divisions
of the ventral rami of L4-L5, S1-S2. These two components can be easily identified as
two separate nerves in about 11% of the cases However, even in those cases the two
components are surrounded by a common sheath. Therefore, this should not be confused
with a true “early” division of the nerve. The real separation of the two components of
the nerve, takes place always in the popliteal fossa.
The nerve comes out of the pelvis through the greater sciatic foramen, entering
the gluteal region anterior to the piriformis muscle and cephalad to the ischial tuberosity.
After reaching the lateral aspect of this bony prominence, the nerve turns vertically
downwards to run between the ischium medially and the greater trochanter laterally, as
shown in figure 7.1.
For most of its trajectory in the buttocks, the sciatic nerve runs parallel to the
midline, at a distance of about 10 cm in adult patients. With the hips in adduction this
distance is maintained throughout adult life, not being influenced by gender or body
weight. This previously unknown fact has simplified enormously the approach to the
sciatic nerve in our practice (see references 5 and 10).
The nerve enters the thigh deep to the biceps femoris muscle. In the thigh, the
position of the nerve with respect to the midline is influenced both by the degree of hip
abduction as well as by the amount of fat accumulating in the inner thigh.
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The nerve runs in the posterior thigh under the cover of the hamstring muscles,
until it reaches the popliteal fossa. Upon entering the popliteal fossa, the two nerve
components, peroneal and tibial, finally diverge from each other, having never mixed
their fibers. The posterior tibial nerve continues to run in the direction of the main trunk,
at the center of the fossa. The common peroneal component turns laterally to run just
medial to the biceps tendon.
Subgluteal fold
The fold that defines the buttocks inferiorly is a fold of the skin. It does not
correspond with the lower border of the gluteus maximus muscle, as frequently thought.
In fact the inferior border of this muscle crosses the subgluteal fold diagonally as it runs
laterally to insert in the iliotibial tract (see figure 7-2). Therefore, during a subgluteal
approach to the sciatic nerve, the needle crosses the same planes (fat and gluteus
maximus) than in more proximal approaches, although the fat layer can be thinner.
Anesthesia of the posterior cutaneous nerve of the thigh is not reliable at this level,
because this nerve usually is already superficial (above the fascia) at the subgluteal fold.
Genitofemoral nerve
It derives from the ventral rami of spinal nerves L1-L2. It provides some of the
innervation of the genital area, part of the medial upper thigh and the skin over the
femoral vessels.
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Saphenous nerve
It is a sensory nerve that originates from the posterior division of the femoral
nerve (L3-L4) in the inguinal region. It is the largest cutaneous branch of the femoral
nerve. It runs down, along with the femoral vessels, under the cover of the sartorius
muscle. It emerges on the medial side of the knee between the tendons of sartorius and
gracilis. At a variable point caudal to the knee joint, it pierces the deep fascia to become
superficial. Below the knee it gives off the subpatellar branch, which supplies the medial
side of the knee (chance for injury during knee arthroscopy). Once it becomes superficial,
it runs alongside the greater saphenous vein in the leg, passing in front of the medial
malleolus, before terminating around the base of the first metatarsal.
Clinical pearls
• The nerves of the lower extremity are distant from each other, making it
impossible to block the entire extremity from a single injection point.
• The position of the sciatic nerve in the buttocks with respect to the midline is
not affected by gender or obesity. Its relationship to bone structures and to the
midline remains unchanged throughout adulthood.
• The inferior border of the gluteus maximus muscle does not correspond with
the subgluteal fold (Snell’s Clinical Anatomy for Medical Students, 3rd
edition, page 554). In fact both cross each other diagonally. The subgluteal
fold is a fold of the skin anchored to the deep fascia. The inferior border of the
gluteus maximus muscle goes diagonally from medial superior to lateral
inferior to insert in the iliotibial tract.
• The gluteus maximus is the only gluteal muscle to cover the sciatic nerve
superficially, caudal to the piriformis muscle. Gluteus medius and minimus
are located cephalad and lateral to the sciatic nerve.
• The inguinal crease does not correspond deep with the inguinal ligament. Both
structures are parallel to each other. The inguinal crease runs about 1 inch (2.5
cm) caudal and parallel to the inguinal ligament.
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LATERAL FEMORAL CUTANEOUS NERVE BLOCK
Indications
This block can be performed alone to provide anesthesia of the lateral thigh (e.g.,
donor area for a skin graft). It can also be performed along with femoral, obturator and
sciatic blocks to provide anesthesia of the thigh for surgical procedures above the knee
and for thigh tourniquet. It is also one of the nerves targeted in a “3-in-1” block, a block
of the femoral nerve performed with a higher volume of local anesthetic, that aims to
block also the lateral femoral and obturator nerves (not supported by the evidence).
Main characteristics
This can be a superficial block (above the fascia lata) if the block is performed at
2 or more cm distal to the inguinal ligament. More proximally the nerve is under the
fascia lata. This is important because this fascia is thick enough to slow the transfer of
local anesthetic to the target nerve.
Technique
The needle entrance point is identified about 1 cm medial and 1 cm caudal to the
ASIS. The needle is advanced perpendicular to the skin and directed deep to the fascia
where the local anesthetic is injected in a fanwise fashion. A nerve stimulator with pulse
duration of 0.3 to 1 ms (300 to 1000 μsec) can be used to elicit a paresthesia in the lateral
thigh.
Complications
Very rare. Some patients can complain of dysesthesia in the area from minor
injury to the nerve. It usually goes away without sequelae.
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FEMORAL NERVE BLOCK
Indications
An isolated femoral nerve block can be performed to provide anesthesia for
surgery on the anterior thigh, patella and some knee procedures. It is more commonly
performed along with sciatic to provide anesthesia of the entire lower extremity. It is also
the point of injection for a “3-in-1” block.
Main characteristics
This is a simple block performed lateral to the pulse of the femoral artery, deep to
the fascia lata (deep fascia of the thigh) and deep to the fascia iliaca (the fascia that
covers the iliopsoas muscle). The femoral artery pulse usually provides an easy and
reliable landmark to the nerve. Ultrasound provides usually an excellent image of the
nerve and neighboring vascular structures facilitating any technique to block it.
Ultrasound technique
The femoral nerve is relatively superficial in most of patients. As usual, use a high
frequency probe (more than 12 MHz) to define structures expected to be at less than 3 cm
of depth. For deeper structures use less than 10 MHz of frequency which provides deeper
penetration and less resolution.
A linear probe at 13-15 MHz can usually provide a good image of the femoral
nerve and vessels. The probe is placed parallel to the inguinal crease, The needle can be
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advanced out of plane with the image of nerve in cross section. The needle can also be
advanced in plane with the probe from lateral to medial. The femoral vein is the most
medial structure of the neurovascular bundle and is easily collapsible by the probe. The
artery is just lateral to the vein. The nerve is lateral to the artery. There is usually a gap of
about 1 cm in between.
Complications
Very rare. Hematomas from puncture of the femoral artery are possible, but
avoidable with meticulous technique, use of small gauge needles and thorough
compression of the arterial puncture when it occurs. The use of ultrasound almost
eliminates this problem.
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OBTURATOR NERVE BLOCK
Indications
It is rarely performed alone. It is more often combined with femoral, lateral
femoral and/or sciatic blocks.
Main characteristics
This is a deep block that requires good anatomical knowledge.
Technique
A 4”, insulated needle connected to a nerve stimulator is advanced perpendicular
to the frontal plane. A local twitch from the pectineus and or adductor longus is usually
obtained. This is just a direct muscle twitch. Deep to this level, the tip of the needle
should reach the nerve eliciting thigh adduction. The current is lowered to 0.5 mA, and if
a twitch is still visible, a slow injection is started. If the needle makes contact with the
pubis ramus, it is walked off caudally.
Complications
Hematoma is the most frequent complication of this technique. Adductor muscles
spasm can occur.
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LUMBAR PLEXUS BLOCK (alternatively called “psoas compartment block”)
Indications
Its goal is to produce anesthesia of the lateral femoral, femoral and obturator
nerves, so it can be used along with sciatic nerve to provide anesthesia of the entire lower
extremity. It is also used to provide postoperative analgesia after hip and knee surgery.
Main characteristics
It is the posterior approach of a “3-in-1” block. It is a deep block, in which the
needle goes through several layers, including subcutaneous tissue, the mass of paraspinal
muscles, and the quadratus lumborum muscle before ending just superficial to the psoas
muscle, in the retroperitoneal space.
Because of the depth at which the nerves are located, the operator has little
control over the exact location of the needle tip, increasing the potential risk for
complications. It is essential that the operator be familiar with the anatomy. The epidural,
subdural and intrathecal spaces are very close to the trajectory of the needle and so is the
kidney and the iliac vessels. Cases of penetration of the peritoneal cavity with injury of
the contents have been reported.
This block should not be performed in obese patients.
Ultrasound technique
This is a deep block. Some people use a curved 4-5 MHz probe to delineate the
psoas and the anatomy of the lumbar plexus, but it is challenging. We do not perform it
routinely.
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Local anesthetic and volume
A volume of 30-40 mL of 1% mepivacaine or 0.5% ropivacaine can be used. For
analgesia the concentration is lowered.
Complications
This is the regional anesthesia technique associated with the highest amount of
complications. Retroperitoneal hematomas, subdural and intrathecal injection, total
spinal, as well as kidney and bowel punctures have been reported.
Clinical pearls
• This is a deep block with important potential complications. It is not a block for
the novice.
• The anesthesiologist must carefully balance the potential benefits against the risks
of complications.
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SCIATIC NERVE BLOCK
Classic approach (Labat as modified by Winnie)
Indications
As an isolated block, it provides anesthesia of the back of the thigh (through
anesthesia of the posterior cutaneous nerve of the thigh, a branch of the sacral plexus) and
most of the lower extremity below the knee, with the exception of the medial side of the
leg (saphenous nerve). If used along with femoral, lateral femoral and obturator nerve
blocks (lumbar plexus block), it completes the anesthesia of the entire lower extremity.
Main characteristics
Labat’s approach is a highly anatomical approach, that requires the identification
of the posterior superior iliac spine (PSIS) and the greater trochanter (GT). A dissection
of the gluteal area shows that this is an accurate approach if the operator is able to
accurately determine the actual position of the PSIS and GT, disregarding ANY soft
tissue (i.e., muscle, bursa, subcutaneous tissue).
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nerve located closer to the midline than a shorter patient. This obviously could not be the
case. The fact is that the perpendicular line of Labat was not created to be flexible in
length.
The combined “classic” approach (Labat-Winnie), despite its shortcomings, is the
most commonly used posterior approach to the sciatic nerve in the gluteal area.
Technique
Usually the block can be completed with a 4”, insulated needle, but sometimes a
longer needle needs to be used. The needle is advanced, perpendicular to all planes until a
twitch from the sciatic nerve is found. If a twitch is still visible at 0.5 mA a slow injection
is started with frequent aspirations. If the nerve is not contacted, the technique does not
have a clear strategy for reposition of the needle. In fact the nerve could be at any point
around a 360-degree radius.
Complications
The literature mentions that the absorption from this site is minimal. However, it
is important to remember that the branches of the inferior gluteal vessels at this level are
large and multiple, therefore hematomas could develop. The patient lying supine
immediately post block could theoretically help.
It is important to inject slowly, alternated with frequent and gentle aspirations.
Dysesthesias in the territories of the sciatic or posterior femoral cutaneous nerves are
reported more frequently after this block than any other. These usually resolve within 1-2
weeks.
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SCIATIC NERVE BLOCK
Franco’s approach
Indications
The same indications than for a classic technique.
Main characteristics
This is a simple technique that relies on one simple anatomical landmark, the
intergluteal sulcus (midline), making the palpation of any buried landmarks totally
unnecessary. It is based on simple, although not universally known facts:
1. The trajectory of the sciatic nerve in the gluteal region is for the most part parallel
to the midline.
2. The width of the adult pelvis is similar in all adults and “surprisingly” similar in
males and females at any given age. Variation in hip width reflects a hormone-
dependent, gender-related different pattern of fat deposition. In fact most of the
differences in the human bony pelvis are limited to the inner pelvis. Thicker bones
in the males compensate for the wider inner pelvis of females to make the average
bicrestal diameter (total width) 280 mm in males and 275 mm in females.
3. The sciatic nerve is about 10 cm from the midline (intergluteal sulcus) in all
adults. What remains highly variable is the depth at which the nerve is located and
the distance from the nerve to the lateral side of the patient. However, the distance
midline-nerve is dictated by the distance midline-ischium. As the bony pelvis
stops growing, this distance becomes fixed and unaffected by soft tissue.
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The patient is placed in the lateral position with both hips and knees slightly
flexed. In a true lateral decubitus, a tangential line to the buttocks, should form a 90-
degree angle with the table. Having the patient placed at straight angles with the table,
makes his/her midline parallel to the table. The midpoint of the intergluteal sulcus, from
top to bottom, is identified. From this point, the needle insertion point is marked at 10 cm
lateral to it (see figure 7-3). This is a linear measurement that, on purpose, disregards any
particular curvature or contour in the patient’s buttocks. The insertion point, always
located at 10 cm from the midline, can be moved distally at will, as far caudal as the
subgluteal fold. This could be necessary for example, if the buttock is large and the
needle is not long enough.
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the twitch. If the twitch becomes too weak, before reaching 0.5 mA, the current is not
lowered any further and instead the operator slowly moves the needle closer to the nerve.
It is not infrequent to see the response fade as the needle is inserted deeper. This
can be the result of a needle approaching the nerve tangentially, along one of the sides of
the nerve. We usually try to perform a small correction in order to get a “bull’s eye”
alignment with the nerve. Deciding whether to correct lateral or medial depends on what
type of response is being elicited. Eversion and dorsiflexion are responses from the
common peroneal nerve (lateral side), while inversion and plantar flexion are responses
from the tibial nerve (medial side). A small correction is then made accordingly. A more
controlled correction can be accomplished by only partially removing the needle a couple
of cm. The unburied portion of the needle is then bent and directed in the desired
direction. The buried portion of the needle keeps the needle from overcorrecting.
Bringing the needle out completely, and then reinserting it, carries a chance of
overshooting the correction.
Ultrasound technique
The nerve is identified in cross section as usual. Because of the sciatic nerve
depth, usually a curved 5-7 MHz probe is needed. The needle can be advanced cephalad
out of plane. Injecting small amounts of local anesthetic helps to localize the tip of the
needle.
Complications
Same as classic approach.
Pearls
• The 10 cm measurement is a linear measurement that disregards, on purpose, the
patient’s buttock contour. This linear measurement tries to reflect only the
distance between the midline and the outer lip of the ischium, without soft tissue
interference.
• Placing the patient in true lateral position, makes the patient’s midline parallel to
the table. If this position is not possible, the operator needs to ascertain the degree
of inclination of the midline with respect to the table, so the needle still may be
advanced parallel to the patient’s midline.
• When the nerve is not found at first attempt, it could only be located either lateral
or medial to the needle. Because of gravity, it is more frequent to underestimate
the midline-nerve distance (sagging midline). Therefore, the first correction
should be lateral.
• When reposition is necessary, keep in mind the “vector” effect. At a theoretical
distance of 9 cm a 10-degree correction will move the needle app 1.6 cm. A 20-
degree correction will move it 3.4 cm. This big “jump” could easily overshoot the
correction. A small 10-degree correction usually is all it takes to localize the
nerve.
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SCIATIC NERVE BLOCK, SUBGLUTEAL
di Benedetto’s approach
Indications
This is a block more suitable for surgery below the knee, because it does not
reliably block the posterior femoral cutaneous nerve (back of the thigh). It can also be
used for continuous catheter techniques.
Main characteristics
There are several techniques performed at or around the subgluteal fold. Some
authors mention Raj’s “supine approach” to sciatic nerve (Anesthesia & Analgesia 1975)
as being the first. In fact, this is a sciatic block performed between the ischium and
greater trochanter (mid-gluteal, not subgluteal level), just a few cm caudal to Labat’s
classic approach. In this technique the extremity is elevated and flexed at the hip and
knee, stretching the buttock tissues. This supposedly brings the sciatic nerve closer to the
skin. It is interesting to note that, even though this technique is universally known as
“Raj’s supine approach”, a completely similar technique was published a year earlier
(1974) by Winnie and colleagues in Anesthesiology Review. Raj’s technique was
correctly devised “for below-the-knee operations”. This fact is frequently forgotten and
we will revisit it later.
A popular infra or subgluteal technique is the technique introduced by di
Benedetto and colleagues in 2001.
1. Ischium and greater trochanter are located at about the same tranverse plane in the
buttocks, as shown in figure 7-1. Di Benedetto’s perpendicular line going caudal
and lateral, needs to have the trochanter located significantly higher than the
ischium.
2. The subgluteal fold is about 8 cm caudal to the midpoint between ischium and
greater trochanter and not 4 cm. On the other hand, being the subgluteal fold so
evident, would it suffice to extend the line until it intercepted the subgluteal fold?
3. At the subgluteal fold the three components of the hamstring muscles are
practically fused together in one single tendon, without any evident groove in
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between. More distally in the thigh a groove can be found between biceps and
semitendinosus, but it is too subtle to be easily palpable through several layers of
tissue (skin, subcutaneous tissue and thick fascia lata).
4. A groove is visible in most people between the biceps and the iliotibial tract. This
groove has nothing to do with the trajectory of the sciatic nerve.
5. The sciatic nerve runs under the biceps femoris and not in a groove between
biceps and semitendinosus.
Technique
The authors advice to insert the needle perpendicular to the skin until a twitch
from the sciatic nerve is obtained.
Complications
Common to other approaches to the sciatic nerve.
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SCIATIC NERVE BLOCK, SUBGLUTEAL
Franco’s approach
The subgluteal approach can be easily performed at 10 cm from the midline at the
subgluteal fold, with the patient lying in lateral decubitus, as shown in fig 7-4.
The 10-cm measurement is made lateral to the midline at the level of the
subgluteal fold, in a way similar to the one described for the mid-gluteal approach. The
needle is advanced parallel to the midline, through the gluteus maximus muscle and into
the sciatic nerve. The current is lowered to around 0.5 mA and a slow injection is started.
If the nerve is missed at first pass it could only be located medial or lateral to the needle.
The needle is reinserted, with a small 10-degree correction in its orientation, first lateral
(toward the trochanter) and then medial (to the midline) if necessary.
Ultrasound technique
Although the same tissue layers cover the sciatic nerve at the midgluteal and
subgluteal levels, the fat layer is usually thinner. This makes the ultrasound visualization
of the sciatic nerve at this level more likely. Depending on depth, the nerve could be
visualized with a linear high frequency probe, but frequently a lower frequency probe is
needed. Curved low frequency probes are needed for bigger patients. The patient is
placed prone or in lateral position. The nerve is visualized in cross section and the needle
is advanced either out of plane or in line with the probe.
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3. The sciatic nerve is relatively more superficial at the subgluteal fold because the
amount of fat decreases from mid-gluteal to subgluteal level, although the type of
layers (fat and muscle) remains the same.
4. The popliteal fossa is the only level in the trajectory of the sciatic nerve in which
the nerve is not covered superficially by muscle. Approaching the sciatic nerve,
without passing through muscle is the only true advantage of a popliteal approach.
5. In terms of anesthesia distribution, the subgluteal approach is more comparable to
the popliteal block than to other more proximal approaches.
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SCIATIC NERVE BLOCK, POPLITEAL
Franco’s approach
Indications
It is especially suitable for foot surgery. Along with femoral nerve block
(saphenous) it provides complete anesthesia below the knee.
Main characteristics
This is the only place in the trajectory of the sciatic nerve where the nerve is not
covered superficially by muscle, perhaps the only true advantage over other more
proximal approaches to the sciatic nerve. Characteristically, a sciatic block done at this
level has a slower onset and lower success rate than more proximal approaches. The fact
that the two components of the nerve diverge from each other could account for some of
the partial blocks. However, slower onset and lower success are sometimes observed in
cases where there is reasonable evidence to believe that the main trunk has been
contacted. One of the possible reasons is that the nerve sheath fuses with the fat that fills
the popliteal fossa. The fat of the popliteal fossa would “soak” away the local anesthetic,
“stealing” it from the nerve surroundings.
Ultrasound technique
Patient is prone. A linear high frequency probe can be used, but a lower frequency
probe is usually needed. The probe is placed across the fossa to obtain a cross section of
vessels and nerves. It is easier to start scanning at the popliteal crease, where the two
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nerve components are more superficial. The probe is then moved cephalad from the
popliteal crease to identify the point at which both components come together. An
alternative method is to find the common peroneal division just medial to the biceps
tendon at the crease and follow it proximally toward the main sciatic trunk.
Complications
Small hematoma can develop. Residual dysesthesia lasting up to two weeks can
be seen.
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POPLITEAL BLOCK, LATERAL APPROACH
Indications
It is especially suitable for any surgery below the knee including ankle and foot,
in patients who cannot be placed in any other position than supine
Main characteristics
Blocking the sciatic nerve with this approach is a little bit more challenging than
the posterior approach. Biceps and vastus lateralis fibers are in close physical contact so
the needle usually stimulates some muscle fibers before reaching the sciatic nerve.
Ultrasound technique
The patient is placed prone with a slight rotation to the opposite side. The probe is
placed across in the popliteal fossa facing anterior. A cross section of the sciatic nerve is
obtained. The needle is advanced from the lateral side, in plane with the probe.
Complications
The same than for posterior approach.
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References
1. Snell RS: Clinical anatomy for medical students, 3rd edition. Boston, MA: Little,
Brown and Company; 1986
2. Shipman P, Walker A, Bichell D: Human skeleton. Cambridge, MA: Harvard
University Press; 1985
3. Hall J, Froster-Iskenius U, Allanton J: Handbook of normal physical
measurements. Oxford: Oxford University Press; 1989
4. Labat G: Regional anesthesia: Its technique and clinical application. Philadelphia,
PA: W.B. Saunders, 1922
5. Winnie A, Ramamurthy S, Durrani Z, et al. Plexus blocks for lower extremity
surgery. Anesthesiology Review 1974; 1: 11-16
6. Franco, CD. Posterior approach to the sciatic nerve in adults: Is Euclidean
geometry still necessary? Anesthesiology 2003; 98: 723-728
7. Di Benedetto P, Bertini L, Casati A, et al. A new approach to the sciatic nerve
block: A prospective, randomized comparison with the classic posterior approach.
Anesth Analg 2001; 93: 1040-1044
8. Rogers J, Ramamurthy S: Lower extremity blocks, Regional anesthesia and
analgesia. Edited by Brown DL. Philadelphia, PA: W.B. Saunders Company,
1996
9. Mulroy M: Regional Anesthesia, An illustrated procedural guide, 3rd edition.
Philadelphia, PA: Lippincott Williams & Wilkins; 2002
10. Enneking FK, Chan V, Greger J, et al. Lower-extremity peripheral nerve
blockade: Essentials of our current understanding. Reg Anesth Pain Med 2005;
30: 4-35
11. Franco CD, Choksi N, Rahman A, Voronov G, Almachnouk M. A Subgluteal
Approach to the Sciatic Nerve in Adults at 10 cm from the Midline. Reg Anesth
Pain Med 2006; 31: 215-20
12. Cunningham’s Textbook of Anatomy, 5th edition. Edited by Robinson A. New
York, William Wood and Company, 1928, pp 258
13. Hollinshead’s Textbook of Anatomy, 5th edition. Edited by Rosse C, Gaddum-
Rosse P. Philadelphia, Lippincott-Raven, 1997, pp 641–80
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CHAPTER 8
CONTINUOUS NERVE BLOCKS
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Introduction
Continuous techniques
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a high success rate. Catheters techniques (“secondary block”) do not generally achieve
the same degree of success. Catheters need to be closely placed in the proximity of target
nerve(s) in order to decrease the “secondary block failure”, a failure to achieve the same
degree of success than single shot techniques. In general catheters should not be
advanced more than 3-4 cm because the risks for catheter-related complications (e.g.,
knotting, vascular puncture, nerve injury, etc) potentially increase.
The most common problems with catheters include inability to achieve adequate
analgesia and other technical problems like accidental dislodgement and peri-catheter
leaks. Catheters tend to have a “mind of their own”. They can advance away from nerves
and into undesirable places. Capdevila et al in 2005 in a multicenter study that included
1,416 patients identified 17.9 % of “technical problems due to catheters and devices”.
Many techniques are used to increase the resistance to accidental dislodgement.
Perhaps the most successful is the subcutaneous tunnelization of the catheter. It does not
only increase the resistance to removal but also provides the opportunity to direct the
catheter away from the surgical site.
Severe nerve damage and infection are rare complications of continuous
techniques.
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References
1. Ansbro FP. A method of continuous brachial plexus block. Am J Surg 1946; 71:
716-722
2. Selander D. Catheter technique in axillary plexus block. Acta Anaesthesiol Scand
1977; 21: 324-329
3. Liu SS, Salinas FV. Continuous plexus and peripheral nerve blocks for postoperative
analgesia. Anesth Analg 2003; 96: 263-272
4. Boezaart AP: Continuos Peripheral Nerve Blocks, In: Boezaart AP (ed): Anesthesia
and Orthopaedic Surgery. New York, McGraw-Hill, 2006, pp 257-264
5. Capdevila X, Pirat P, Bringuier S, et al. Continuous peripheral nerve blocks in
hospital wards after orthopedic surgery: A multicenter prospective analysis of the
quality of postoperative analgesia in 1,416 patients. Anesthesiology 2005; 103:
1035-1045
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